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anti foxp3 antibody  (Proteintech)


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    Structured Review

    Proteintech anti foxp3 antibody
    Anti Foxp3 Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 150 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/foxp3/FOXP3+Antibody/pm42858252-1016-274-276
    Average 96 stars, based on 150 article reviews
    anti foxp3 antibody - by Bioz Stars, 2026-11
    96/100 stars

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    Related Articles

    Software:

    Article Title: Danggui Shaoyao San ameliorates neuroinflammation in a D-galactose-induced Alzheimer’s disease rat model by suppressing the JAK2/STAT3 pathway and modulating Th17/Treg -related immune dysregulation
    Article Snippet: .. Other reagents included sodium pentobarbital (Merck KGaA, Germany, #P3761), donepezil hydrochloride (MCE, United States, #HY-B0034), D-galactose (Sigma-Aldrich, Shanghai, China, #V900922), primary antibodies targeting STAT3 and Foxp3 (Proteintech, Wuhan, China, #102532-AP, #22228-1-AP), ROR-γt and p-STAT3-Y705 antibodies (HUABIO, Hangzhou, China, #HA722121, #ET1603-40), JAK2 antibody (Aifang, Hunan, China, #AFRM99330), p-JAK2-Y1007/1008 antibody (ABclonal, Wuhan, China, #AP0531), β-actin antibody (Affinity Biosciences, China, #AF7018), postsynaptic density protein 95 (PSD95) and synaptophysin I antibody (abcam, Cambridge, United Kingdom, #ab18258,#ab254349), secondary antibodies (Elabscience, Wuhan, China, #E-AB-1003), Iba1 antibody (Wako Pure Chemical Industries, Ltd., Japan, #011-27991), primers for β-actin, IL-1β, IL-6, etc., were designed using Primer 6.0 software based on sequences from the NCBI database and synthesized by Sangon Biotech (Shanghai), China, reverse transcription kit (Novoprotein, Suzhou, China, #E047-01B), SYBR Mixture premix and RIPA protein lysis buffer (Comwin Biotech, Jiangsu, China, #CW3008M, #CW2333S), ELISA kits (Jianglai Biotechnology, Shanghai, China, #JL13427, #JL20880), BCA protein concentration assay kit (Elabscience Biotechnology, Wuhan, China, #E-BC-K318-M), TRIzol, SlowFadeTM Gold Antifade Mountant with DAPI, and donkey anti-goat Alexa Fluor 647 fluorescent secondary antibody (red) (Thermo Fisher Scientific, United States, #15596-026, # S36942 , #A32849), universal two-step detection kit (Zhongshan Golden Bridge, Beijing, China, #PV-9000), Toluidine blue, Triton X-100, and antifade mounting medium with DAPI (Solarbio Science & Technology Co., Ltd., Beijing, China, #G3663, #T8200, #S2110), hematoxylin staining solution and eosin staining solution (Zhongshan Golden Bridge Biotechnology Co., Ltd., Beijing, China, #ZLI-9610, #ZLI-9613), Fixation/permeabilization kits, dyes, and antibodies against CD4, Foxp3, and IL-17A for phenotypic analysis of Th17 and Treg cells were purchased from BD Pharmingen (United States), detailed information is provided in . ..

    Synthesized:

    Article Title: Danggui Shaoyao San ameliorates neuroinflammation in a D-galactose-induced Alzheimer’s disease rat model by suppressing the JAK2/STAT3 pathway and modulating Th17/Treg -related immune dysregulation
    Article Snippet: .. Other reagents included sodium pentobarbital (Merck KGaA, Germany, #P3761), donepezil hydrochloride (MCE, United States, #HY-B0034), D-galactose (Sigma-Aldrich, Shanghai, China, #V900922), primary antibodies targeting STAT3 and Foxp3 (Proteintech, Wuhan, China, #102532-AP, #22228-1-AP), ROR-γt and p-STAT3-Y705 antibodies (HUABIO, Hangzhou, China, #HA722121, #ET1603-40), JAK2 antibody (Aifang, Hunan, China, #AFRM99330), p-JAK2-Y1007/1008 antibody (ABclonal, Wuhan, China, #AP0531), β-actin antibody (Affinity Biosciences, China, #AF7018), postsynaptic density protein 95 (PSD95) and synaptophysin I antibody (abcam, Cambridge, United Kingdom, #ab18258,#ab254349), secondary antibodies (Elabscience, Wuhan, China, #E-AB-1003), Iba1 antibody (Wako Pure Chemical Industries, Ltd., Japan, #011-27991), primers for β-actin, IL-1β, IL-6, etc., were designed using Primer 6.0 software based on sequences from the NCBI database and synthesized by Sangon Biotech (Shanghai), China, reverse transcription kit (Novoprotein, Suzhou, China, #E047-01B), SYBR Mixture premix and RIPA protein lysis buffer (Comwin Biotech, Jiangsu, China, #CW3008M, #CW2333S), ELISA kits (Jianglai Biotechnology, Shanghai, China, #JL13427, #JL20880), BCA protein concentration assay kit (Elabscience Biotechnology, Wuhan, China, #E-BC-K318-M), TRIzol, SlowFadeTM Gold Antifade Mountant with DAPI, and donkey anti-goat Alexa Fluor 647 fluorescent secondary antibody (red) (Thermo Fisher Scientific, United States, #15596-026, # S36942 , #A32849), universal two-step detection kit (Zhongshan Golden Bridge, Beijing, China, #PV-9000), Toluidine blue, Triton X-100, and antifade mounting medium with DAPI (Solarbio Science & Technology Co., Ltd., Beijing, China, #G3663, #T8200, #S2110), hematoxylin staining solution and eosin staining solution (Zhongshan Golden Bridge Biotechnology Co., Ltd., Beijing, China, #ZLI-9610, #ZLI-9613), Fixation/permeabilization kits, dyes, and antibodies against CD4, Foxp3, and IL-17A for phenotypic analysis of Th17 and Treg cells were purchased from BD Pharmingen (United States), detailed information is provided in . ..

    Reverse Transcription:

    Article Title: Danggui Shaoyao San ameliorates neuroinflammation in a D-galactose-induced Alzheimer’s disease rat model by suppressing the JAK2/STAT3 pathway and modulating Th17/Treg -related immune dysregulation
    Article Snippet: .. Other reagents included sodium pentobarbital (Merck KGaA, Germany, #P3761), donepezil hydrochloride (MCE, United States, #HY-B0034), D-galactose (Sigma-Aldrich, Shanghai, China, #V900922), primary antibodies targeting STAT3 and Foxp3 (Proteintech, Wuhan, China, #102532-AP, #22228-1-AP), ROR-γt and p-STAT3-Y705 antibodies (HUABIO, Hangzhou, China, #HA722121, #ET1603-40), JAK2 antibody (Aifang, Hunan, China, #AFRM99330), p-JAK2-Y1007/1008 antibody (ABclonal, Wuhan, China, #AP0531), β-actin antibody (Affinity Biosciences, China, #AF7018), postsynaptic density protein 95 (PSD95) and synaptophysin I antibody (abcam, Cambridge, United Kingdom, #ab18258,#ab254349), secondary antibodies (Elabscience, Wuhan, China, #E-AB-1003), Iba1 antibody (Wako Pure Chemical Industries, Ltd., Japan, #011-27991), primers for β-actin, IL-1β, IL-6, etc., were designed using Primer 6.0 software based on sequences from the NCBI database and synthesized by Sangon Biotech (Shanghai), China, reverse transcription kit (Novoprotein, Suzhou, China, #E047-01B), SYBR Mixture premix and RIPA protein lysis buffer (Comwin Biotech, Jiangsu, China, #CW3008M, #CW2333S), ELISA kits (Jianglai Biotechnology, Shanghai, China, #JL13427, #JL20880), BCA protein concentration assay kit (Elabscience Biotechnology, Wuhan, China, #E-BC-K318-M), TRIzol, SlowFadeTM Gold Antifade Mountant with DAPI, and donkey anti-goat Alexa Fluor 647 fluorescent secondary antibody (red) (Thermo Fisher Scientific, United States, #15596-026, # S36942 , #A32849), universal two-step detection kit (Zhongshan Golden Bridge, Beijing, China, #PV-9000), Toluidine blue, Triton X-100, and antifade mounting medium with DAPI (Solarbio Science & Technology Co., Ltd., Beijing, China, #G3663, #T8200, #S2110), hematoxylin staining solution and eosin staining solution (Zhongshan Golden Bridge Biotechnology Co., Ltd., Beijing, China, #ZLI-9610, #ZLI-9613), Fixation/permeabilization kits, dyes, and antibodies against CD4, Foxp3, and IL-17A for phenotypic analysis of Th17 and Treg cells were purchased from BD Pharmingen (United States), detailed information is provided in . ..

    Lysis:

    Article Title: Danggui Shaoyao San ameliorates neuroinflammation in a D-galactose-induced Alzheimer’s disease rat model by suppressing the JAK2/STAT3 pathway and modulating Th17/Treg -related immune dysregulation
    Article Snippet: .. Other reagents included sodium pentobarbital (Merck KGaA, Germany, #P3761), donepezil hydrochloride (MCE, United States, #HY-B0034), D-galactose (Sigma-Aldrich, Shanghai, China, #V900922), primary antibodies targeting STAT3 and Foxp3 (Proteintech, Wuhan, China, #102532-AP, #22228-1-AP), ROR-γt and p-STAT3-Y705 antibodies (HUABIO, Hangzhou, China, #HA722121, #ET1603-40), JAK2 antibody (Aifang, Hunan, China, #AFRM99330), p-JAK2-Y1007/1008 antibody (ABclonal, Wuhan, China, #AP0531), β-actin antibody (Affinity Biosciences, China, #AF7018), postsynaptic density protein 95 (PSD95) and synaptophysin I antibody (abcam, Cambridge, United Kingdom, #ab18258,#ab254349), secondary antibodies (Elabscience, Wuhan, China, #E-AB-1003), Iba1 antibody (Wako Pure Chemical Industries, Ltd., Japan, #011-27991), primers for β-actin, IL-1β, IL-6, etc., were designed using Primer 6.0 software based on sequences from the NCBI database and synthesized by Sangon Biotech (Shanghai), China, reverse transcription kit (Novoprotein, Suzhou, China, #E047-01B), SYBR Mixture premix and RIPA protein lysis buffer (Comwin Biotech, Jiangsu, China, #CW3008M, #CW2333S), ELISA kits (Jianglai Biotechnology, Shanghai, China, #JL13427, #JL20880), BCA protein concentration assay kit (Elabscience Biotechnology, Wuhan, China, #E-BC-K318-M), TRIzol, SlowFadeTM Gold Antifade Mountant with DAPI, and donkey anti-goat Alexa Fluor 647 fluorescent secondary antibody (red) (Thermo Fisher Scientific, United States, #15596-026, # S36942 , #A32849), universal two-step detection kit (Zhongshan Golden Bridge, Beijing, China, #PV-9000), Toluidine blue, Triton X-100, and antifade mounting medium with DAPI (Solarbio Science & Technology Co., Ltd., Beijing, China, #G3663, #T8200, #S2110), hematoxylin staining solution and eosin staining solution (Zhongshan Golden Bridge Biotechnology Co., Ltd., Beijing, China, #ZLI-9610, #ZLI-9613), Fixation/permeabilization kits, dyes, and antibodies against CD4, Foxp3, and IL-17A for phenotypic analysis of Th17 and Treg cells were purchased from BD Pharmingen (United States), detailed information is provided in . ..

    Enzyme-linked Immunosorbent Assay:

    Article Title: Danggui Shaoyao San ameliorates neuroinflammation in a D-galactose-induced Alzheimer’s disease rat model by suppressing the JAK2/STAT3 pathway and modulating Th17/Treg -related immune dysregulation
    Article Snippet: .. Other reagents included sodium pentobarbital (Merck KGaA, Germany, #P3761), donepezil hydrochloride (MCE, United States, #HY-B0034), D-galactose (Sigma-Aldrich, Shanghai, China, #V900922), primary antibodies targeting STAT3 and Foxp3 (Proteintech, Wuhan, China, #102532-AP, #22228-1-AP), ROR-γt and p-STAT3-Y705 antibodies (HUABIO, Hangzhou, China, #HA722121, #ET1603-40), JAK2 antibody (Aifang, Hunan, China, #AFRM99330), p-JAK2-Y1007/1008 antibody (ABclonal, Wuhan, China, #AP0531), β-actin antibody (Affinity Biosciences, China, #AF7018), postsynaptic density protein 95 (PSD95) and synaptophysin I antibody (abcam, Cambridge, United Kingdom, #ab18258,#ab254349), secondary antibodies (Elabscience, Wuhan, China, #E-AB-1003), Iba1 antibody (Wako Pure Chemical Industries, Ltd., Japan, #011-27991), primers for β-actin, IL-1β, IL-6, etc., were designed using Primer 6.0 software based on sequences from the NCBI database and synthesized by Sangon Biotech (Shanghai), China, reverse transcription kit (Novoprotein, Suzhou, China, #E047-01B), SYBR Mixture premix and RIPA protein lysis buffer (Comwin Biotech, Jiangsu, China, #CW3008M, #CW2333S), ELISA kits (Jianglai Biotechnology, Shanghai, China, #JL13427, #JL20880), BCA protein concentration assay kit (Elabscience Biotechnology, Wuhan, China, #E-BC-K318-M), TRIzol, SlowFadeTM Gold Antifade Mountant with DAPI, and donkey anti-goat Alexa Fluor 647 fluorescent secondary antibody (red) (Thermo Fisher Scientific, United States, #15596-026, # S36942 , #A32849), universal two-step detection kit (Zhongshan Golden Bridge, Beijing, China, #PV-9000), Toluidine blue, Triton X-100, and antifade mounting medium with DAPI (Solarbio Science & Technology Co., Ltd., Beijing, China, #G3663, #T8200, #S2110), hematoxylin staining solution and eosin staining solution (Zhongshan Golden Bridge Biotechnology Co., Ltd., Beijing, China, #ZLI-9610, #ZLI-9613), Fixation/permeabilization kits, dyes, and antibodies against CD4, Foxp3, and IL-17A for phenotypic analysis of Th17 and Treg cells were purchased from BD Pharmingen (United States), detailed information is provided in . ..

    Protein Concentration:

    Article Title: Danggui Shaoyao San ameliorates neuroinflammation in a D-galactose-induced Alzheimer’s disease rat model by suppressing the JAK2/STAT3 pathway and modulating Th17/Treg -related immune dysregulation
    Article Snippet: .. Other reagents included sodium pentobarbital (Merck KGaA, Germany, #P3761), donepezil hydrochloride (MCE, United States, #HY-B0034), D-galactose (Sigma-Aldrich, Shanghai, China, #V900922), primary antibodies targeting STAT3 and Foxp3 (Proteintech, Wuhan, China, #102532-AP, #22228-1-AP), ROR-γt and p-STAT3-Y705 antibodies (HUABIO, Hangzhou, China, #HA722121, #ET1603-40), JAK2 antibody (Aifang, Hunan, China, #AFRM99330), p-JAK2-Y1007/1008 antibody (ABclonal, Wuhan, China, #AP0531), β-actin antibody (Affinity Biosciences, China, #AF7018), postsynaptic density protein 95 (PSD95) and synaptophysin I antibody (abcam, Cambridge, United Kingdom, #ab18258,#ab254349), secondary antibodies (Elabscience, Wuhan, China, #E-AB-1003), Iba1 antibody (Wako Pure Chemical Industries, Ltd., Japan, #011-27991), primers for β-actin, IL-1β, IL-6, etc., were designed using Primer 6.0 software based on sequences from the NCBI database and synthesized by Sangon Biotech (Shanghai), China, reverse transcription kit (Novoprotein, Suzhou, China, #E047-01B), SYBR Mixture premix and RIPA protein lysis buffer (Comwin Biotech, Jiangsu, China, #CW3008M, #CW2333S), ELISA kits (Jianglai Biotechnology, Shanghai, China, #JL13427, #JL20880), BCA protein concentration assay kit (Elabscience Biotechnology, Wuhan, China, #E-BC-K318-M), TRIzol, SlowFadeTM Gold Antifade Mountant with DAPI, and donkey anti-goat Alexa Fluor 647 fluorescent secondary antibody (red) (Thermo Fisher Scientific, United States, #15596-026, # S36942 , #A32849), universal two-step detection kit (Zhongshan Golden Bridge, Beijing, China, #PV-9000), Toluidine blue, Triton X-100, and antifade mounting medium with DAPI (Solarbio Science & Technology Co., Ltd., Beijing, China, #G3663, #T8200, #S2110), hematoxylin staining solution and eosin staining solution (Zhongshan Golden Bridge Biotechnology Co., Ltd., Beijing, China, #ZLI-9610, #ZLI-9613), Fixation/permeabilization kits, dyes, and antibodies against CD4, Foxp3, and IL-17A for phenotypic analysis of Th17 and Treg cells were purchased from BD Pharmingen (United States), detailed information is provided in . ..

    Staining:

    Article Title: Danggui Shaoyao San ameliorates neuroinflammation in a D-galactose-induced Alzheimer’s disease rat model by suppressing the JAK2/STAT3 pathway and modulating Th17/Treg -related immune dysregulation
    Article Snippet: .. Other reagents included sodium pentobarbital (Merck KGaA, Germany, #P3761), donepezil hydrochloride (MCE, United States, #HY-B0034), D-galactose (Sigma-Aldrich, Shanghai, China, #V900922), primary antibodies targeting STAT3 and Foxp3 (Proteintech, Wuhan, China, #102532-AP, #22228-1-AP), ROR-γt and p-STAT3-Y705 antibodies (HUABIO, Hangzhou, China, #HA722121, #ET1603-40), JAK2 antibody (Aifang, Hunan, China, #AFRM99330), p-JAK2-Y1007/1008 antibody (ABclonal, Wuhan, China, #AP0531), β-actin antibody (Affinity Biosciences, China, #AF7018), postsynaptic density protein 95 (PSD95) and synaptophysin I antibody (abcam, Cambridge, United Kingdom, #ab18258,#ab254349), secondary antibodies (Elabscience, Wuhan, China, #E-AB-1003), Iba1 antibody (Wako Pure Chemical Industries, Ltd., Japan, #011-27991), primers for β-actin, IL-1β, IL-6, etc., were designed using Primer 6.0 software based on sequences from the NCBI database and synthesized by Sangon Biotech (Shanghai), China, reverse transcription kit (Novoprotein, Suzhou, China, #E047-01B), SYBR Mixture premix and RIPA protein lysis buffer (Comwin Biotech, Jiangsu, China, #CW3008M, #CW2333S), ELISA kits (Jianglai Biotechnology, Shanghai, China, #JL13427, #JL20880), BCA protein concentration assay kit (Elabscience Biotechnology, Wuhan, China, #E-BC-K318-M), TRIzol, SlowFadeTM Gold Antifade Mountant with DAPI, and donkey anti-goat Alexa Fluor 647 fluorescent secondary antibody (red) (Thermo Fisher Scientific, United States, #15596-026, # S36942 , #A32849), universal two-step detection kit (Zhongshan Golden Bridge, Beijing, China, #PV-9000), Toluidine blue, Triton X-100, and antifade mounting medium with DAPI (Solarbio Science & Technology Co., Ltd., Beijing, China, #G3663, #T8200, #S2110), hematoxylin staining solution and eosin staining solution (Zhongshan Golden Bridge Biotechnology Co., Ltd., Beijing, China, #ZLI-9610, #ZLI-9613), Fixation/permeabilization kits, dyes, and antibodies against CD4, Foxp3, and IL-17A for phenotypic analysis of Th17 and Treg cells were purchased from BD Pharmingen (United States), detailed information is provided in . ..

    Blocking Assay:

    Article Title: STT3A-mediated FCN3 N-glycosylation promotes Treg cell activation to drive hepatocellular carcinoma progression via Wnt/β-catenin
    Article Snippet: Samples were separated on SDS-PAGE gels and transferred to PVDF membranes (#IPVH00010, Millipore, Billerica, MA, USA). .. After blocking with 5% skim milk for 2 h at room temperature, membranes were incubated overnight at 4 °C with primary antibodies against FCN3 (#ABIN521997, 1:2000; Antibodies Online, Aachen, Germany), FOXP3 (#22228-1-AP, 1:500; Proteintech), CD25 (#83896-1-RR, 1:1000; Proteintech), APC (#sc-9998, 1:500; Santa Cruz Biotechnology, Santa Cruz, CA, USA), β-catenin (#66379-1-Ig, 1:5000; Proteintech), phosphorylated β-catenin (p-β-catenin) (#80067-1-RR, 1:1000; Proteintech) or STT3A (#ab320831, 1:20000; Abcam, Cambridge, MA, USA). ..

    Article Title: Salidroside ameliorates experimental autoimmune neuritis by dually modulating neuroinflammation and immune homeostasis via PI3K/AKT signaling
    Article Snippet: .. After blocking with 5% goat serum for 1 h at RT, primary antibodies MBP (1:200, Proteintech), CD68 (1:100, Servicebio), CD3 (1:100, Servicebio), CD206 (1:200, Proteintech), CD86 (1:200, Proteintech), IL-17A (1:200, Proteintech), Foxp3 (1:200, Affinity), p -AKT (1:200, Proteintech), p -IκBα (1:200, Affinity), p -P65 (1:200, Proteintech) diluted in antibody diluent were applied to fully cover the tissue sections. ..

    Incubation:

    Article Title: STT3A-mediated FCN3 N-glycosylation promotes Treg cell activation to drive hepatocellular carcinoma progression via Wnt/β-catenin
    Article Snippet: Samples were separated on SDS-PAGE gels and transferred to PVDF membranes (#IPVH00010, Millipore, Billerica, MA, USA). .. After blocking with 5% skim milk for 2 h at room temperature, membranes were incubated overnight at 4 °C with primary antibodies against FCN3 (#ABIN521997, 1:2000; Antibodies Online, Aachen, Germany), FOXP3 (#22228-1-AP, 1:500; Proteintech), CD25 (#83896-1-RR, 1:1000; Proteintech), APC (#sc-9998, 1:500; Santa Cruz Biotechnology, Santa Cruz, CA, USA), β-catenin (#66379-1-Ig, 1:5000; Proteintech), phosphorylated β-catenin (p-β-catenin) (#80067-1-RR, 1:1000; Proteintech) or STT3A (#ab320831, 1:20000; Abcam, Cambridge, MA, USA). ..

    Article Title: Gordonibacter-associated regulatory T cell dysfunction and S100A11-mediated neural impairment in Hirschsprung's disease: a microbiota-immune-neural axis.
    Article Snippet: WB analysis was conducted using 40 μg of total protein per lane on 4-20% gradient polyacrylamide gels (Epizyme Biotech), followed by transfer to polyvinylidene difluoride (PVDF) membranes. .. Primary antibodies targeting S100A11, TLR4, SOX10, HBA1, HBB, and FOXP3 were incubated overnight at 4°C, with detection achieved through HRP-conjugated secondary antibodies (Proteintech) and enhanced chemiluminescence (ECL; Beyotime Cat# P0018S). .. Band intensities were quantified using Image Lab software (Bio-Rad), with beta-actin serving as the loading control.

    Tissue:

    Article Title: Salidroside ameliorates experimental autoimmune neuritis by dually modulating neuroinflammation and immune homeostasis via PI3K/AKT signaling
    Article Snippet: .. After blocking with 5% goat serum for 1 h at RT, primary antibodies MBP (1:200, Proteintech), CD68 (1:100, Servicebio), CD3 (1:100, Servicebio), CD206 (1:200, Proteintech), CD86 (1:200, Proteintech), IL-17A (1:200, Proteintech), Foxp3 (1:200, Affinity), p -AKT (1:200, Proteintech), p -IκBα (1:200, Affinity), p -P65 (1:200, Proteintech) diluted in antibody diluent were applied to fully cover the tissue sections. ..

    Immunohistochemistry:

    Article Title: ZFP36 and CEBPA are macrophage-associated prognostic biomarkers linked to glomerular endothelial inflammation in ANCA-associated glomerulonephritis.
    Article Snippet: Background: Macrophages are critical in antineutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis (AAGN).. This study investigated macrophage-associated genes (MAGs) ZFP36 and CEBPA in AAGN renal tissue and evaluated their role in glomerular endothelial injury.. Methods: Macrophage infiltration and its association with prognosis were assessed in renal tissues via immunohistochemistry.



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    Phenotypic changes and inflammatory factor secretion of T cells stimulated by cardiac lysate antigens (CLAs). (A) Coculture protocol for dendritic cells (DCs) and T cells. The tolerogenic DCs (tDCs) present antigens to T cells; meanwhile, programmed death ligand 1 binds to programmed cell death protein 1 on T cells and inhibits T cell activation, promoting the phenotypic conversion of T cells to regulatory T cells (Tregs). Furthermore, due to the lack of activation signals such as CD80 and CD86, some T cells exhibit a weak activation state after receiving antigen presentation, and under the regulation of key factors such as interleukin-10 (IL-10) and transforming growth factor-β (TGF-β), they undergo phenotypic transition to Tregs. Under restimulation, tDCs phagocytose antigens and present them to Tregs. Tregs are rapidly activated, express high levels of Forkhead box P3 <t>(FOXP3),</t> and directly inhibit T cell activation, while secreting large amounts of anti-inflammatory factors. (B) Flow cytometry (FC) results for T cell phenotype. (C) Quantification of T cell phenotypes by FC. (D) T cell phenotype immunofluorescence staining results, where blue represents cell nuclei, red represents CD127, and green represents CD4. (E) Expression of interferon-γ (IFN-γ), IL-2, IL-10, and TGF-β after coculture of DCs and T cells. (F) Western blot analysis of the activation status of the mechanistic target of rapamycin (mTOR)-p70S6K-S6 pathway after treatment with Gel@PPM, Rapa, inverse vaccine nanomimics (IVNMs), and Gel@IVNMs under CLA stimulation. (G) The percentage of phosphorylation of mTOR, p70S6K, and S6 was statistically analyzed based on the gray values of the western blot results (compared to the unphosphorylated proteins). Data are presented as means ± SD, with individual points representing biological replicates. Statistical significance is indicated as ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.
    Anti Rat Foxp3 Antibody, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Phenotypic changes and inflammatory factor secretion of T cells stimulated by cardiac lysate antigens (CLAs). (A) Coculture protocol for dendritic cells (DCs) and T cells. The tolerogenic DCs (tDCs) present antigens to T cells; meanwhile, programmed death ligand 1 binds to programmed cell death protein 1 on T cells and inhibits T cell activation, promoting the phenotypic conversion of T cells to regulatory T cells (Tregs). Furthermore, due to the lack of activation signals such as CD80 and CD86, some T cells exhibit a weak activation state after receiving antigen presentation, and under the regulation of key factors such as interleukin-10 (IL-10) and transforming growth factor-β (TGF-β), they undergo phenotypic transition to Tregs. Under restimulation, tDCs phagocytose antigens and present them to Tregs. Tregs are rapidly activated, express high levels of Forkhead box P3 <t>(FOXP3),</t> and directly inhibit T cell activation, while secreting large amounts of anti-inflammatory factors. (B) Flow cytometry (FC) results for T cell phenotype. (C) Quantification of T cell phenotypes by FC. (D) T cell phenotype immunofluorescence staining results, where blue represents cell nuclei, red represents CD127, and green represents CD4. (E) Expression of interferon-γ (IFN-γ), IL-2, IL-10, and TGF-β after coculture of DCs and T cells. (F) Western blot analysis of the activation status of the mechanistic target of rapamycin (mTOR)-p70S6K-S6 pathway after treatment with Gel@PPM, Rapa, inverse vaccine nanomimics (IVNMs), and Gel@IVNMs under CLA stimulation. (G) The percentage of phosphorylation of mTOR, p70S6K, and S6 was statistically analyzed based on the gray values of the western blot results (compared to the unphosphorylated proteins). Data are presented as means ± SD, with individual points representing biological replicates. Statistical significance is indicated as ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.
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    Phenotypic changes and inflammatory factor secretion of T cells stimulated by cardiac lysate antigens (CLAs). (A) Coculture protocol for dendritic cells (DCs) and T cells. The tolerogenic DCs (tDCs) present antigens to T cells; meanwhile, programmed death ligand 1 binds to programmed cell death protein 1 on T cells and inhibits T cell activation, promoting the phenotypic conversion of T cells to regulatory T cells (Tregs). Furthermore, due to the lack of activation signals such as CD80 and CD86, some T cells exhibit a weak activation state after receiving antigen presentation, and under the regulation of key factors such as interleukin-10 (IL-10) and transforming growth factor-β (TGF-β), they undergo phenotypic transition to Tregs. Under restimulation, tDCs phagocytose antigens and present them to Tregs. Tregs are rapidly activated, express high levels of Forkhead box P3 <t>(FOXP3),</t> and directly inhibit T cell activation, while secreting large amounts of anti-inflammatory factors. (B) Flow cytometry (FC) results for T cell phenotype. (C) Quantification of T cell phenotypes by FC. (D) T cell phenotype immunofluorescence staining results, where blue represents cell nuclei, red represents CD127, and green represents CD4. (E) Expression of interferon-γ (IFN-γ), IL-2, IL-10, and TGF-β after coculture of DCs and T cells. (F) Western blot analysis of the activation status of the mechanistic target of rapamycin (mTOR)-p70S6K-S6 pathway after treatment with Gel@PPM, Rapa, inverse vaccine nanomimics (IVNMs), and Gel@IVNMs under CLA stimulation. (G) The percentage of phosphorylation of mTOR, p70S6K, and S6 was statistically analyzed based on the gray values of the western blot results (compared to the unphosphorylated proteins). Data are presented as means ± SD, with individual points representing biological replicates. Statistical significance is indicated as ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.
    Foxp3 Transcription Factor, supplied by Cytek Biosciences, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Phenotypic changes and inflammatory factor secretion of T cells stimulated by cardiac lysate antigens (CLAs). (A) Coculture protocol for dendritic cells (DCs) and T cells. The tolerogenic DCs (tDCs) present antigens to T cells; meanwhile, programmed death ligand 1 binds to programmed cell death protein 1 on T cells and inhibits T cell activation, promoting the phenotypic conversion of T cells to regulatory T cells (Tregs). Furthermore, due to the lack of activation signals such as CD80 and CD86, some T cells exhibit a weak activation state after receiving antigen presentation, and under the regulation of key factors such as interleukin-10 (IL-10) and transforming growth factor-β (TGF-β), they undergo phenotypic transition to Tregs. Under restimulation, tDCs phagocytose antigens and present them to Tregs. Tregs are rapidly activated, express high levels of Forkhead box P3 <t>(FOXP3),</t> and directly inhibit T cell activation, while secreting large amounts of anti-inflammatory factors. (B) Flow cytometry (FC) results for T cell phenotype. (C) Quantification of T cell phenotypes by FC. (D) T cell phenotype immunofluorescence staining results, where blue represents cell nuclei, red represents CD127, and green represents CD4. (E) Expression of interferon-γ (IFN-γ), IL-2, IL-10, and TGF-β after coculture of DCs and T cells. (F) Western blot analysis of the activation status of the mechanistic target of rapamycin (mTOR)-p70S6K-S6 pathway after treatment with Gel@PPM, Rapa, inverse vaccine nanomimics (IVNMs), and Gel@IVNMs under CLA stimulation. (G) The percentage of phosphorylation of mTOR, p70S6K, and S6 was statistically analyzed based on the gray values of the western blot results (compared to the unphosphorylated proteins). Data are presented as means ± SD, with individual points representing biological replicates. Statistical significance is indicated as ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.
    Cells, supplied by Cytek Biosciences, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc foxp3 d2w8e rabbit monoclonal antibody
    Phenotypic changes and inflammatory factor secretion of T cells stimulated by cardiac lysate antigens (CLAs). (A) Coculture protocol for dendritic cells (DCs) and T cells. The tolerogenic DCs (tDCs) present antigens to T cells; meanwhile, programmed death ligand 1 binds to programmed cell death protein 1 on T cells and inhibits T cell activation, promoting the phenotypic conversion of T cells to regulatory T cells (Tregs). Furthermore, due to the lack of activation signals such as CD80 and CD86, some T cells exhibit a weak activation state after receiving antigen presentation, and under the regulation of key factors such as interleukin-10 (IL-10) and transforming growth factor-β (TGF-β), they undergo phenotypic transition to Tregs. Under restimulation, tDCs phagocytose antigens and present them to Tregs. Tregs are rapidly activated, express high levels of Forkhead box P3 <t>(FOXP3),</t> and directly inhibit T cell activation, while secreting large amounts of anti-inflammatory factors. (B) Flow cytometry (FC) results for T cell phenotype. (C) Quantification of T cell phenotypes by FC. (D) T cell phenotype immunofluorescence staining results, where blue represents cell nuclei, red represents CD127, and green represents CD4. (E) Expression of interferon-γ (IFN-γ), IL-2, IL-10, and TGF-β after coculture of DCs and T cells. (F) Western blot analysis of the activation status of the mechanistic target of rapamycin (mTOR)-p70S6K-S6 pathway after treatment with Gel@PPM, Rapa, inverse vaccine nanomimics (IVNMs), and Gel@IVNMs under CLA stimulation. (G) The percentage of phosphorylation of mTOR, p70S6K, and S6 was statistically analyzed based on the gray values of the western blot results (compared to the unphosphorylated proteins). Data are presented as means ± SD, with individual points representing biological replicates. Statistical significance is indicated as ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.
    Foxp3 D2w8e Rabbit Monoclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Phenotypic changes and inflammatory factor secretion of T cells stimulated by cardiac lysate antigens (CLAs). (A) Coculture protocol for dendritic cells (DCs) and T cells. The tolerogenic DCs (tDCs) present antigens to T cells; meanwhile, programmed death ligand 1 binds to programmed cell death protein 1 on T cells and inhibits T cell activation, promoting the phenotypic conversion of T cells to regulatory T cells (Tregs). Furthermore, due to the lack of activation signals such as CD80 and CD86, some T cells exhibit a weak activation state after receiving antigen presentation, and under the regulation of key factors such as interleukin-10 (IL-10) and transforming growth factor-β (TGF-β), they undergo phenotypic transition to Tregs. Under restimulation, tDCs phagocytose antigens and present them to Tregs. Tregs are rapidly activated, express high levels of Forkhead box P3 <t>(FOXP3),</t> and directly inhibit T cell activation, while secreting large amounts of anti-inflammatory factors. (B) Flow cytometry (FC) results for T cell phenotype. (C) Quantification of T cell phenotypes by FC. (D) T cell phenotype immunofluorescence staining results, where blue represents cell nuclei, red represents CD127, and green represents CD4. (E) Expression of interferon-γ (IFN-γ), IL-2, IL-10, and TGF-β after coculture of DCs and T cells. (F) Western blot analysis of the activation status of the mechanistic target of rapamycin (mTOR)-p70S6K-S6 pathway after treatment with Gel@PPM, Rapa, inverse vaccine nanomimics (IVNMs), and Gel@IVNMs under CLA stimulation. (G) The percentage of phosphorylation of mTOR, p70S6K, and S6 was statistically analyzed based on the gray values of the western blot results (compared to the unphosphorylated proteins). Data are presented as means ± SD, with individual points representing biological replicates. Statistical significance is indicated as ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.
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    Phenotypic changes and inflammatory factor secretion of T cells stimulated by cardiac lysate antigens (CLAs). (A) Coculture protocol for dendritic cells (DCs) and T cells. The tolerogenic DCs (tDCs) present antigens to T cells; meanwhile, programmed death ligand 1 binds to programmed cell death protein 1 on T cells and inhibits T cell activation, promoting the phenotypic conversion of T cells to regulatory T cells (Tregs). Furthermore, due to the lack of activation signals such as CD80 and CD86, some T cells exhibit a weak activation state after receiving antigen presentation, and under the regulation of key factors such as interleukin-10 (IL-10) and transforming growth factor-β (TGF-β), they undergo phenotypic transition to Tregs. Under restimulation, tDCs phagocytose antigens and present them to Tregs. Tregs are rapidly activated, express high levels of Forkhead box P3 <t>(FOXP3),</t> and directly inhibit T cell activation, while secreting large amounts of anti-inflammatory factors. (B) Flow cytometry (FC) results for T cell phenotype. (C) Quantification of T cell phenotypes by FC. (D) T cell phenotype immunofluorescence staining results, where blue represents cell nuclei, red represents CD127, and green represents CD4. (E) Expression of interferon-γ (IFN-γ), IL-2, IL-10, and TGF-β after coculture of DCs and T cells. (F) Western blot analysis of the activation status of the mechanistic target of rapamycin (mTOR)-p70S6K-S6 pathway after treatment with Gel@PPM, Rapa, inverse vaccine nanomimics (IVNMs), and Gel@IVNMs under CLA stimulation. (G) The percentage of phosphorylation of mTOR, p70S6K, and S6 was statistically analyzed based on the gray values of the western blot results (compared to the unphosphorylated proteins). Data are presented as means ± SD, with individual points representing biological replicates. Statistical significance is indicated as ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.
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    Image Search Results


    BPNSs gavage ameliorated arthritis by remodeling Treg/Th17 imbalance. (A) Detailed schematic of the animal experimental procedures of CIA PBS and CIA BPNSs groups. (B) Arthritis scores in CIA mice. (C) Representative photographs and micro-CT images of paws. (D) Quantitative analyses of bone histomorphometry indexes including BMD, BV/TV, Tb.Th, Tb.Sp, and Tb.N in CIA mice. (E) Representative histology images of joints. Scale bar, 100 μm. (F) Histological scores of the joints. (G) Representative TRAP staining images of joints. Scale bar, 100 μm. (H) Quantitative analyses of TRAP staining. (I–N) Flow cytometric analysis and quantification of IL-17A⁺ Th17 cells and FOXP3⁺ Treg cells among CD4⁺ T cells, as well as the Treg/Th17 ratio, in the spleen, MLN and DLN. (O–S) Flow cytometric analysis and quantification of MDSC-like cells, G-MDSC-like cells and M-MDSC-like cells in the spleen. (T) The expression of CD11c, MHCII and CD86 of MDSC-like cells in spleen detected by flow cytometry and statistically analyzed. (U) Immunofluorescence staining of ZO-1 and Occludin in colon tissue. Scale bar, 100 μm. (V) MFI quantification of ZO-1 and Occludin after normalization. (W) Volcano plot of differentially abundant serum inflammatory proteins in CIA BPNSs versus CIA PBS , as determined by a mouse inflammation antibody array. ns, p ≥ 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Journal: Gut Microbes

    Article Title: Targeted intestinal ROS scavenging alleviated rheumatoid arthritis by microbial metabolite kynurenic acid mediated Treg/Th17 balance through AhR pathway activation

    doi: 10.1080/19490976.2026.2739669

    Figure Lengend Snippet: BPNSs gavage ameliorated arthritis by remodeling Treg/Th17 imbalance. (A) Detailed schematic of the animal experimental procedures of CIA PBS and CIA BPNSs groups. (B) Arthritis scores in CIA mice. (C) Representative photographs and micro-CT images of paws. (D) Quantitative analyses of bone histomorphometry indexes including BMD, BV/TV, Tb.Th, Tb.Sp, and Tb.N in CIA mice. (E) Representative histology images of joints. Scale bar, 100 μm. (F) Histological scores of the joints. (G) Representative TRAP staining images of joints. Scale bar, 100 μm. (H) Quantitative analyses of TRAP staining. (I–N) Flow cytometric analysis and quantification of IL-17A⁺ Th17 cells and FOXP3⁺ Treg cells among CD4⁺ T cells, as well as the Treg/Th17 ratio, in the spleen, MLN and DLN. (O–S) Flow cytometric analysis and quantification of MDSC-like cells, G-MDSC-like cells and M-MDSC-like cells in the spleen. (T) The expression of CD11c, MHCII and CD86 of MDSC-like cells in spleen detected by flow cytometry and statistically analyzed. (U) Immunofluorescence staining of ZO-1 and Occludin in colon tissue. Scale bar, 100 μm. (V) MFI quantification of ZO-1 and Occludin after normalization. (W) Volcano plot of differentially abundant serum inflammatory proteins in CIA BPNSs versus CIA PBS , as determined by a mouse inflammation antibody array. ns, p ≥ 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Article Snippet: For naïve CD4+ T cells cultured under Treg-polarizing conditions, the following primary antibodies were used: p-mTOR (Ser2448) (Zenbio, Cat. no. 381557, 1:1,000), mTOR (Abmart, Cat. no. T55306F, 1:500), p-p70 S6 kinase (Thr389) (Cell Signaling Technology, Cat. no. 9205, 1:200), p70 S6 kinase (Zenbio, Cat. no. R25650 , 1:1,000), p-AKT (Ser473) (Zenbio, Cat. no. 310021, 1:500), AKT (Zenbio, Cat. no. R23411 , 1:500), p-4E-BP1 (Thr46) (Zenbio, Cat. no. R22929 , 1:1,000), 4E-BP1 (Zenbio, Cat. no. R24197 , 1:500) and FOXP3 (Bioss, Cat. no. bs-10211R, 1:500).

    Techniques: Micro-CT, Histology, Staining, Analysis, Expressing, Flow Cytometry, Immunofluorescence, Tissue, Ab Array

    Gut microbiota depletion led to a reduction in the efficacy of BPNSs. (A) Detailed schematic of the animal experimental procedures of CIA ABX and CIA ABX+BPNSs groups. (B) Arthritis scores in CIA mice. (C) Representative photographs and micro-CT images of paws. (D) Quantitative analyses of bone histomorphometry indexes including BMD, BV/TV, Tb.Th, Tb.Sp, and Tb.N in CIA mice. (E) Representative histology images of joints. Scale bar, 100 μm. (F) Histological scores of joints. (G) Representative TRAP staining images of joints. Scale bar, 100 μm. (H) Quantitative analyses of TRAP staining. (I–L) Flow cytometric analysis and quantification of IL-17A⁺ Th17 cells and FOXP3⁺ Treg cells among CD4⁺ T cells, as well as the Treg/Th17 ratio, in the spleen and MLN. ns, p ≥ 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Journal: Gut Microbes

    Article Title: Targeted intestinal ROS scavenging alleviated rheumatoid arthritis by microbial metabolite kynurenic acid mediated Treg/Th17 balance through AhR pathway activation

    doi: 10.1080/19490976.2026.2739669

    Figure Lengend Snippet: Gut microbiota depletion led to a reduction in the efficacy of BPNSs. (A) Detailed schematic of the animal experimental procedures of CIA ABX and CIA ABX+BPNSs groups. (B) Arthritis scores in CIA mice. (C) Representative photographs and micro-CT images of paws. (D) Quantitative analyses of bone histomorphometry indexes including BMD, BV/TV, Tb.Th, Tb.Sp, and Tb.N in CIA mice. (E) Representative histology images of joints. Scale bar, 100 μm. (F) Histological scores of joints. (G) Representative TRAP staining images of joints. Scale bar, 100 μm. (H) Quantitative analyses of TRAP staining. (I–L) Flow cytometric analysis and quantification of IL-17A⁺ Th17 cells and FOXP3⁺ Treg cells among CD4⁺ T cells, as well as the Treg/Th17 ratio, in the spleen and MLN. ns, p ≥ 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Article Snippet: For naïve CD4+ T cells cultured under Treg-polarizing conditions, the following primary antibodies were used: p-mTOR (Ser2448) (Zenbio, Cat. no. 381557, 1:1,000), mTOR (Abmart, Cat. no. T55306F, 1:500), p-p70 S6 kinase (Thr389) (Cell Signaling Technology, Cat. no. 9205, 1:200), p70 S6 kinase (Zenbio, Cat. no. R25650 , 1:1,000), p-AKT (Ser473) (Zenbio, Cat. no. 310021, 1:500), AKT (Zenbio, Cat. no. R23411 , 1:500), p-4E-BP1 (Thr46) (Zenbio, Cat. no. R22929 , 1:1,000), 4E-BP1 (Zenbio, Cat. no. R24197 , 1:500) and FOXP3 (Bioss, Cat. no. bs-10211R, 1:500).

    Techniques: Micro-CT, Histology, Staining, Analysis

    Fecal transplantation from BPNSs-administered CIA mice ameliorated arthritis. (A) Detailed schematic of the animal experimental procedures of CIA FMT-CIA+PBS and CIA FMT-CIA+BPNSs groups. (B) Arthritis scores in CIA mice. (C Representative photographs and micro-CT images of paws. (D) Quantitative analyses of bone histomorphometry indexes including BMD, BV/TV, Tb.Th, Tb.Sp, and Tb.N in CIA mice. (E) Representative histology images of joints. Scale bar, 100 μm. (F) Histological scores of the joints. (G) Representative TRAP staining images of joints. Scale bar, 100 μm. (H) Quantitative analyses of TRAP staining. (I–L) Flow cytometric analysis and quantification of IL-17A⁺ Th17 cells and FOXP3⁺ Treg cells among CD4⁺ T cells, as well as the Treg/Th17 ratio, in the spleen and MLN. ns, p ≥ 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Journal: Gut Microbes

    Article Title: Targeted intestinal ROS scavenging alleviated rheumatoid arthritis by microbial metabolite kynurenic acid mediated Treg/Th17 balance through AhR pathway activation

    doi: 10.1080/19490976.2026.2739669

    Figure Lengend Snippet: Fecal transplantation from BPNSs-administered CIA mice ameliorated arthritis. (A) Detailed schematic of the animal experimental procedures of CIA FMT-CIA+PBS and CIA FMT-CIA+BPNSs groups. (B) Arthritis scores in CIA mice. (C Representative photographs and micro-CT images of paws. (D) Quantitative analyses of bone histomorphometry indexes including BMD, BV/TV, Tb.Th, Tb.Sp, and Tb.N in CIA mice. (E) Representative histology images of joints. Scale bar, 100 μm. (F) Histological scores of the joints. (G) Representative TRAP staining images of joints. Scale bar, 100 μm. (H) Quantitative analyses of TRAP staining. (I–L) Flow cytometric analysis and quantification of IL-17A⁺ Th17 cells and FOXP3⁺ Treg cells among CD4⁺ T cells, as well as the Treg/Th17 ratio, in the spleen and MLN. ns, p ≥ 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Article Snippet: For naïve CD4+ T cells cultured under Treg-polarizing conditions, the following primary antibodies were used: p-mTOR (Ser2448) (Zenbio, Cat. no. 381557, 1:1,000), mTOR (Abmart, Cat. no. T55306F, 1:500), p-p70 S6 kinase (Thr389) (Cell Signaling Technology, Cat. no. 9205, 1:200), p70 S6 kinase (Zenbio, Cat. no. R25650 , 1:1,000), p-AKT (Ser473) (Zenbio, Cat. no. 310021, 1:500), AKT (Zenbio, Cat. no. R23411 , 1:500), p-4E-BP1 (Thr46) (Zenbio, Cat. no. R22929 , 1:1,000), 4E-BP1 (Zenbio, Cat. no. R24197 , 1:500) and FOXP3 (Bioss, Cat. no. bs-10211R, 1:500).

    Techniques: Transplantation Assay, Micro-CT, Histology, Staining, Analysis

    KYNA promoted Treg cell differentiation by suppressing mTORC1 activation through the AhR pathway. (A) Predicted binding mode of KYNA within the ligand-binding pocket of AhR. (B) The expression of FOXP3 in naïve CD4⁺ T cells cultured under TGF-β-induced conditions with different concentrations of KYNA, in the presence or absence of CH-223191, was detected by flow cytometry. (C) GSEA of the PI3K/AKT signaling pathway between the control and KYNA-treated groups. (D) Representative Western blot images of AKT, p-AKT, mTOR, p-mTOR, p70 S6K, p-p70 S6K, 4E-BP1, p-4E-BP1, and FOXP3 in the presence or absence of KYNA. (E) Western blot quantification of AKT, p-AKT, mTOR, p-mTOR, p70 S6K, p-p70 S6K, 4E-BP1, p-4E-BP1, and FOXP3 protein levels (normalized to β-actin). ns, p ≥ 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Journal: Gut Microbes

    Article Title: Targeted intestinal ROS scavenging alleviated rheumatoid arthritis by microbial metabolite kynurenic acid mediated Treg/Th17 balance through AhR pathway activation

    doi: 10.1080/19490976.2026.2739669

    Figure Lengend Snippet: KYNA promoted Treg cell differentiation by suppressing mTORC1 activation through the AhR pathway. (A) Predicted binding mode of KYNA within the ligand-binding pocket of AhR. (B) The expression of FOXP3 in naïve CD4⁺ T cells cultured under TGF-β-induced conditions with different concentrations of KYNA, in the presence or absence of CH-223191, was detected by flow cytometry. (C) GSEA of the PI3K/AKT signaling pathway between the control and KYNA-treated groups. (D) Representative Western blot images of AKT, p-AKT, mTOR, p-mTOR, p70 S6K, p-p70 S6K, 4E-BP1, p-4E-BP1, and FOXP3 in the presence or absence of KYNA. (E) Western blot quantification of AKT, p-AKT, mTOR, p-mTOR, p70 S6K, p-p70 S6K, 4E-BP1, p-4E-BP1, and FOXP3 protein levels (normalized to β-actin). ns, p ≥ 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Article Snippet: For naïve CD4+ T cells cultured under Treg-polarizing conditions, the following primary antibodies were used: p-mTOR (Ser2448) (Zenbio, Cat. no. 381557, 1:1,000), mTOR (Abmart, Cat. no. T55306F, 1:500), p-p70 S6 kinase (Thr389) (Cell Signaling Technology, Cat. no. 9205, 1:200), p70 S6 kinase (Zenbio, Cat. no. R25650 , 1:1,000), p-AKT (Ser473) (Zenbio, Cat. no. 310021, 1:500), AKT (Zenbio, Cat. no. R23411 , 1:500), p-4E-BP1 (Thr46) (Zenbio, Cat. no. R22929 , 1:1,000), 4E-BP1 (Zenbio, Cat. no. R24197 , 1:500) and FOXP3 (Bioss, Cat. no. bs-10211R, 1:500).

    Techniques: Cell Differentiation, Activation Assay, Binding Assay, Ligand Binding Assay, Expressing, Cell Culture, Flow Cytometry, Control, Western Blot

    KYNA exerted anti-rheumatic arthritis effects in vivo through the AhR pathway. (A) Detailed schematic of the animal experimental procedures of CIA PBS , CIA KYNA and CIA KYNA+CH-223191 groups. (B) Arthritis scores in CIA mice. (C) Representative photographs and micro-CT images of paws. (D) Quantitative analyses of bone histomorphometry indexes including BMD, BV/TV, Tb.Th, Tb.Sp, and Tb.N in CIA mice. (E) Representative HE staining images of joints. Scale bar, 100 μm. (F) Histological scores of the joints. (G) Representative TRAP staining images of joints. Scale bar, 100 μm. (H) Quantitative analyses of TRAP staining. (I–L) Flow cytometric analysis and quantification of IL-17A⁺ Th17 cells and FOXP3⁺ Treg cells among CD4⁺ T cells, as well as the Treg/Th17 ratio, in the spleen and MLN. (M–P) (M and O), Representative immunofluorescence staining of ZO-1 and Occludin in colon tissue. Scale bar, 100 μm. (N and P) Quantification of the MFI of ZO-1 and Occludin after normalization. (Q) Representative Western blot images of ZO-1 and Occludin in the presence of KYNA or KYNA + CH-223191 in IEC-6 cells. (R and S) Western blot quantification of ZO-1 and Occludin protein levels (normalized to β-actin). ns, p ≥ 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Journal: Gut Microbes

    Article Title: Targeted intestinal ROS scavenging alleviated rheumatoid arthritis by microbial metabolite kynurenic acid mediated Treg/Th17 balance through AhR pathway activation

    doi: 10.1080/19490976.2026.2739669

    Figure Lengend Snippet: KYNA exerted anti-rheumatic arthritis effects in vivo through the AhR pathway. (A) Detailed schematic of the animal experimental procedures of CIA PBS , CIA KYNA and CIA KYNA+CH-223191 groups. (B) Arthritis scores in CIA mice. (C) Representative photographs and micro-CT images of paws. (D) Quantitative analyses of bone histomorphometry indexes including BMD, BV/TV, Tb.Th, Tb.Sp, and Tb.N in CIA mice. (E) Representative HE staining images of joints. Scale bar, 100 μm. (F) Histological scores of the joints. (G) Representative TRAP staining images of joints. Scale bar, 100 μm. (H) Quantitative analyses of TRAP staining. (I–L) Flow cytometric analysis and quantification of IL-17A⁺ Th17 cells and FOXP3⁺ Treg cells among CD4⁺ T cells, as well as the Treg/Th17 ratio, in the spleen and MLN. (M–P) (M and O), Representative immunofluorescence staining of ZO-1 and Occludin in colon tissue. Scale bar, 100 μm. (N and P) Quantification of the MFI of ZO-1 and Occludin after normalization. (Q) Representative Western blot images of ZO-1 and Occludin in the presence of KYNA or KYNA + CH-223191 in IEC-6 cells. (R and S) Western blot quantification of ZO-1 and Occludin protein levels (normalized to β-actin). ns, p ≥ 0.05; * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Article Snippet: For naïve CD4+ T cells cultured under Treg-polarizing conditions, the following primary antibodies were used: p-mTOR (Ser2448) (Zenbio, Cat. no. 381557, 1:1,000), mTOR (Abmart, Cat. no. T55306F, 1:500), p-p70 S6 kinase (Thr389) (Cell Signaling Technology, Cat. no. 9205, 1:200), p70 S6 kinase (Zenbio, Cat. no. R25650 , 1:1,000), p-AKT (Ser473) (Zenbio, Cat. no. 310021, 1:500), AKT (Zenbio, Cat. no. R23411 , 1:500), p-4E-BP1 (Thr46) (Zenbio, Cat. no. R22929 , 1:1,000), 4E-BP1 (Zenbio, Cat. no. R24197 , 1:500) and FOXP3 (Bioss, Cat. no. bs-10211R, 1:500).

    Techniques: In Vivo, Micro-CT, H&E Stain, Staining, Analysis, Immunofluorescence, Tissue, Western Blot

    Schematic illustration of the protective mechanism of BPNSs against RA progression. The ROS scavenger BPNSs remodeled the gut microbiota, altered KYNA levels, and promoted Treg cell differentiation via the AhR-AKT-mTOR signaling pathway, thereby ameliorating RA progression. Created in https://BioRender.com .

    Journal: Gut Microbes

    Article Title: Targeted intestinal ROS scavenging alleviated rheumatoid arthritis by microbial metabolite kynurenic acid mediated Treg/Th17 balance through AhR pathway activation

    doi: 10.1080/19490976.2026.2739669

    Figure Lengend Snippet: Schematic illustration of the protective mechanism of BPNSs against RA progression. The ROS scavenger BPNSs remodeled the gut microbiota, altered KYNA levels, and promoted Treg cell differentiation via the AhR-AKT-mTOR signaling pathway, thereby ameliorating RA progression. Created in https://BioRender.com .

    Article Snippet: For naïve CD4+ T cells cultured under Treg-polarizing conditions, the following primary antibodies were used: p-mTOR (Ser2448) (Zenbio, Cat. no. 381557, 1:1,000), mTOR (Abmart, Cat. no. T55306F, 1:500), p-p70 S6 kinase (Thr389) (Cell Signaling Technology, Cat. no. 9205, 1:200), p70 S6 kinase (Zenbio, Cat. no. R25650 , 1:1,000), p-AKT (Ser473) (Zenbio, Cat. no. 310021, 1:500), AKT (Zenbio, Cat. no. R23411 , 1:500), p-4E-BP1 (Thr46) (Zenbio, Cat. no. R22929 , 1:1,000), 4E-BP1 (Zenbio, Cat. no. R24197 , 1:500) and FOXP3 (Bioss, Cat. no. bs-10211R, 1:500).

    Techniques: Cell Differentiation

    Phenotypic changes and inflammatory factor secretion of T cells stimulated by cardiac lysate antigens (CLAs). (A) Coculture protocol for dendritic cells (DCs) and T cells. The tolerogenic DCs (tDCs) present antigens to T cells; meanwhile, programmed death ligand 1 binds to programmed cell death protein 1 on T cells and inhibits T cell activation, promoting the phenotypic conversion of T cells to regulatory T cells (Tregs). Furthermore, due to the lack of activation signals such as CD80 and CD86, some T cells exhibit a weak activation state after receiving antigen presentation, and under the regulation of key factors such as interleukin-10 (IL-10) and transforming growth factor-β (TGF-β), they undergo phenotypic transition to Tregs. Under restimulation, tDCs phagocytose antigens and present them to Tregs. Tregs are rapidly activated, express high levels of Forkhead box P3 (FOXP3), and directly inhibit T cell activation, while secreting large amounts of anti-inflammatory factors. (B) Flow cytometry (FC) results for T cell phenotype. (C) Quantification of T cell phenotypes by FC. (D) T cell phenotype immunofluorescence staining results, where blue represents cell nuclei, red represents CD127, and green represents CD4. (E) Expression of interferon-γ (IFN-γ), IL-2, IL-10, and TGF-β after coculture of DCs and T cells. (F) Western blot analysis of the activation status of the mechanistic target of rapamycin (mTOR)-p70S6K-S6 pathway after treatment with Gel@PPM, Rapa, inverse vaccine nanomimics (IVNMs), and Gel@IVNMs under CLA stimulation. (G) The percentage of phosphorylation of mTOR, p70S6K, and S6 was statistically analyzed based on the gray values of the western blot results (compared to the unphosphorylated proteins). Data are presented as means ± SD, with individual points representing biological replicates. Statistical significance is indicated as ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

    Journal: Research

    Article Title: Inverse Vaccine Nanomimics: In situ Antigen-Specific Immune Tolerance Induction for Durable Cardiac Repair Post-Myocardial Infarction

    doi: 10.34133/research.1464

    Figure Lengend Snippet: Phenotypic changes and inflammatory factor secretion of T cells stimulated by cardiac lysate antigens (CLAs). (A) Coculture protocol for dendritic cells (DCs) and T cells. The tolerogenic DCs (tDCs) present antigens to T cells; meanwhile, programmed death ligand 1 binds to programmed cell death protein 1 on T cells and inhibits T cell activation, promoting the phenotypic conversion of T cells to regulatory T cells (Tregs). Furthermore, due to the lack of activation signals such as CD80 and CD86, some T cells exhibit a weak activation state after receiving antigen presentation, and under the regulation of key factors such as interleukin-10 (IL-10) and transforming growth factor-β (TGF-β), they undergo phenotypic transition to Tregs. Under restimulation, tDCs phagocytose antigens and present them to Tregs. Tregs are rapidly activated, express high levels of Forkhead box P3 (FOXP3), and directly inhibit T cell activation, while secreting large amounts of anti-inflammatory factors. (B) Flow cytometry (FC) results for T cell phenotype. (C) Quantification of T cell phenotypes by FC. (D) T cell phenotype immunofluorescence staining results, where blue represents cell nuclei, red represents CD127, and green represents CD4. (E) Expression of interferon-γ (IFN-γ), IL-2, IL-10, and TGF-β after coculture of DCs and T cells. (F) Western blot analysis of the activation status of the mechanistic target of rapamycin (mTOR)-p70S6K-S6 pathway after treatment with Gel@PPM, Rapa, inverse vaccine nanomimics (IVNMs), and Gel@IVNMs under CLA stimulation. (G) The percentage of phosphorylation of mTOR, p70S6K, and S6 was statistically analyzed based on the gray values of the western blot results (compared to the unphosphorylated proteins). Data are presented as means ± SD, with individual points representing biological replicates. Statistical significance is indicated as ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

    Article Snippet: After surface staining, cells were fixed and permeabilized with Fixation/Permeabilization Concentrate and Permeabilization Buffer (E-CK-A108, Elabscience, China) according to the manufacturer’s instructions and intracellularly stained with an anti-rat FOXP3 antibody (E-AB-F1351J, Elabscience, China).

    Techniques: Activation Assay, Immunopeptidomics, Flow Cytometry, Immunofluorescence, Staining, Expressing, Western Blot, Analysis, Phospho-proteomics

    Changes in dendritic cell phenotype and regulatory T cell responses in cardiac-draining lymph nodes after myocardial infarction (MI). (A) Representative flow cytometry plots showing CD11c + MHC-II + dendritic cells and programmed death ligand 1 (PD-L1) expression in the Control, Gel@PPM, Gel@PP@Rapa, Gel@OVA-IVNMs, and Gel@IVNMs groups at 7 and 56 d after MI. (B) Quantification of the proportion of PD-L1 + cells within the CD11c + MHC-II + dendritic cell population at 7 and 56 d. (C) Quantification of CD4 + CD25 + FOXP3 + regulatory T cells (Tregs) in lymph node-derived cells from the 5 treatment groups after 48 h of culture under unstimulated Control, OVA, or cardiac lysate antigen (CLA) stimulation at 7 and 56 d. (D) Representative flow cytometry plots of CD25 and Forkhead box P3 (FOXP3) expression within CD4 + T cells in the Gel@OVA-IVNMs and Gel@IVNMs groups following Control, OVA, or CLA stimulation at 7 and 56 d. Data are presented as means ± SD, with individual points representing biological replicates. Statistical significance is indicated as ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

    Journal: Research

    Article Title: Inverse Vaccine Nanomimics: In situ Antigen-Specific Immune Tolerance Induction for Durable Cardiac Repair Post-Myocardial Infarction

    doi: 10.34133/research.1464

    Figure Lengend Snippet: Changes in dendritic cell phenotype and regulatory T cell responses in cardiac-draining lymph nodes after myocardial infarction (MI). (A) Representative flow cytometry plots showing CD11c + MHC-II + dendritic cells and programmed death ligand 1 (PD-L1) expression in the Control, Gel@PPM, Gel@PP@Rapa, Gel@OVA-IVNMs, and Gel@IVNMs groups at 7 and 56 d after MI. (B) Quantification of the proportion of PD-L1 + cells within the CD11c + MHC-II + dendritic cell population at 7 and 56 d. (C) Quantification of CD4 + CD25 + FOXP3 + regulatory T cells (Tregs) in lymph node-derived cells from the 5 treatment groups after 48 h of culture under unstimulated Control, OVA, or cardiac lysate antigen (CLA) stimulation at 7 and 56 d. (D) Representative flow cytometry plots of CD25 and Forkhead box P3 (FOXP3) expression within CD4 + T cells in the Gel@OVA-IVNMs and Gel@IVNMs groups following Control, OVA, or CLA stimulation at 7 and 56 d. Data are presented as means ± SD, with individual points representing biological replicates. Statistical significance is indicated as ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

    Article Snippet: After surface staining, cells were fixed and permeabilized with Fixation/Permeabilization Concentrate and Permeabilization Buffer (E-CK-A108, Elabscience, China) according to the manufacturer’s instructions and intracellularly stained with an anti-rat FOXP3 antibody (E-AB-F1351J, Elabscience, China).

    Techniques: Flow Cytometry, Expressing, Control, Derivative Assay