Journal: Bioactive Materials

Article Title: Chronic inflammation-responsive hydrogel restores myeloid-T cell crosstalk to reinvigorate antitumor immunity against metastatic colorectal cancer

doi: 10.1016/j.bioactmat.2026.03.012

Figure Lengend Snippet: PGE2 blockade modulates immune cell phenotypes in antitumor resp onses. (A) Inflammatory gene expression across cancer types (GEPIA2 database). (B) Gene expression of Il1b , Cxcl8 , and Lif in colon adenocarcinoma (COAD) tumor tissue and normal tissue (GEPIA2 database). (C and D) Correlation between Ptgs2 and inflammatory genes in various cancers (C) and COAD (D) (TIMER 2.0). (E) Schematic of immune cells co-incubated with CXB treated tumor conditional medium (TCM) (Source material from BioRender). (F and G) Cell viability (F) and Cell cycle arrest (G) detection of CT26 tumor cells treated with gradient concentrations of CXB; n = 3. (H) PGE2 concentration in CT26 cell supernatants; n = 3. (I) The proportion of CD103 + DC within BMDCs after CXB treatments in vitro ; n = 3. (J and K) Maturation (J) and Antigen processing capability (K) on BMDCs; n = 3. (L – N) Flow charts of CD86 or CD206 expression on Raw 264.7 cells (L). Quantification of CD86 (M) and CD206 (N) expression on Raw 264.7 cells; n = 3. (O and P) Flow charts (O) and Quantification (P) of CD69 and CD137 expression on splenic T cells exposed to CXB-pretreated TCM; n = 3. (Q) IFN-γ secretion by T cells co-cultured with CXB-pretreated TCM; n = 3. Data are presented as mean ± SD, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Significance was calculated using One-way ANOVA.

Article Snippet: CT26 cells and Raw 264.7 were purchased from the American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Gene Expression, Incubation, Concentration Assay, In Vitro, Expressing, Cell Culture

Journal: Bioactive Materials

Article Title: Chronic inflammation-responsive hydrogel restores myeloid-T cell crosstalk to reinvigorate antitumor immunity against metastatic colorectal cancer

doi: 10.1016/j.bioactmat.2026.03.012

Figure Lengend Snippet: Sustained PGE2 blockade prompts immune activ ation. (A) Structure of hydrogel matrix and scheme of Gel-CXB preparation (Source material from BioRender). (B) Microstructure of the hydrogel. (C) Rheological evaluation of Gel-CXB. (D) CXB release from Gel-CXB in PBS or PBS containing 0.5 mM H 2 O 2 ; n = 3. (E and F) Flow chart (E) and Quantification (F) of CD103 + DC within BMDCs; n = 3. (G and H) Flow chart (G) and Heatmap (H) of costimulatory molecular expression on CD103 - DC, CD103 + DC, or total DC with different treatments; n = 3. (I and J) CXCL9 (I) and Costimulatory molecular expression (J) on cDC1; n = 3. (K – M) CD86 and CD206 expression (K), MHC-II expression (L), and Antigen processing capability (M) of BMDMs incubated with different TCM; n = 3. (N and O) CD69 (N) and CD137 (O) expression on CD8 + T cells co-incubated with different TCM; n = 3. (P) Scheme of Gel-CXB-regulated CT26 TME at different time points in vivo . (Q) Changes of several immune cells within TME at Day 1, 5, and 9; n = 3. (R) Tumor volume of mice treated with CXB alone or Gel-CXB in vivo ; n = 5. (S) CD137 expression on CD8 + T cells in vivo ; n = 3. Data are presented as mean ± SD, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Significance was calculated using One-way ANOVA.

Article Snippet: CT26 cells and Raw 264.7 were purchased from the American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Expressing, Incubation, In Vivo

Journal: Bioactive Materials

Article Title: Chronic inflammation-responsive hydrogel restores myeloid-T cell crosstalk to reinvigorate antitumor immunity against metastatic colorectal cancer

doi: 10.1016/j.bioactmat.2026.03.012

Figure Lengend Snippet: TRANS inhibits tumor growth and enhances local and systemic immune resp onses. (A) Scheme of GC, GCF, or TRANS preparation (Source material from BioRender). (B) Microstructure of GC and TRANS. (C) Experimental design for administration and immune cell analysis. (D) Tumor growth curves under different treatments; n = 5. (E) Tumor weight post-treatment; n = 5. (F – H) CD45 + leukocytes and CD11c + DCs (F), CD86 + M1 and CD206 + M2 macrophages (G), and Tumor-infiltrating CD8 + T cells (H) within TME; n = 5. (I – L) Mature DCs (I), CD8α + cDC1s (J), CD4 + and CD8 + T cells (K) and CD69 + CD8 + T cells (L) in lymph nodes; n = 5. (M – Q) CD11c + MHC II + DCs (M), CD8α + cDC1s (N), CD4 + and CD8 + T cells (O), CD69 + CD8 + T cells (P), and IFN-γ + CD8 + T cells (Q) in the spleen; n = 5. (R – T) CD8 + T cells (R), The ratio of CD8 + T /CD4 + T cells (S), and IFN-γ levels (T) in blood; n = 5. (U) IFN-γ + CD4 + T and IFN-γ + CD8 + T cells with ex vivo stimulation of PMA/ionomycin for 6 h; n = 3. (V) Apoptosis of CT26 cells co-incubated with splenic T cells for 24 h; n = 3. Data are presented as mean ± SD, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Significance was calculated using One-way ANOVA.

Article Snippet: CT26 cells and Raw 264.7 were purchased from the American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Cell Analysis, Ex Vivo, Incubation

Journal: Bioactive Materials

Article Title: Chronic inflammation-responsive hydrogel restores myeloid-T cell crosstalk to reinvigorate antitumor immunity against metastatic colorectal cancer

doi: 10.1016/j.bioactmat.2026.03.012

Figure Lengend Snippet: TRANS inhibits tumor metastasis and induces immune memory in vivo . (A) Experimental design for secondary tumor model. (B and C) Tumor volume curves of primary tumor (B) and secondary tumor (C) during different therapy; n = 5. (D and E) Statistical diagram (D) and flow charts (E) of T cells within secondary tumors; n = 5. (F) Immunofluorescence images of immune cell in primary tumor. (G) Schematic of lung metastasis tumor model and treatment regimen. Mice received subcutaneous and intravenous injections of CT26-Luc. (H – J) In vivo images (H), Primary tumor volume curves (I), and Average radiance in lungs (J) of CT26-Luc tumor-bearing mice; n = 5. (K – M) Lung image (K), Lung metastasis foci counts and weights (L), and H&E staining of lungs (M) from CT26-Luc tumor-bearing mice; n = 5. (N) Schematic of liver metastasis tumor model and treatment regimen. Mice received subcutaneous CT26 tumor and splenic CT26-Luc injections. (O and P) In vivo imaging (O) and Individual radiance in livers (P) of CT26-Luc tumor-bearing mice; n = 10. (Q – S) Live images (Q), Liver weights (R), and H&E staining images of livers (S) from PBS- or TRANS-treated mice; n = 5. (T) Scheme of tumor rechallenge model. (U) Tumor changes in mice rechallenged with CT26 or 4T1; n = 9. (V) Central memory (T CM ) and effector memory (T EM ) gated on CD8 + T cells; n = 5. Data are presented as mean ± SD, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Significance was calculated using One-way ANOVA.

Article Snippet: CT26 cells and Raw 264.7 were purchased from the American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: In Vivo, Immunofluorescence, Staining, In Vivo Imaging

Journal: iScience

Article Title: Triple-armed oncolytic HSV enhances antitumor immunity by remodeling the tumor microenvironment in subcutaneous murine CRC

doi: 10.1016/j.isci.2026.115883

Figure Lengend Snippet: oHSV-1 exhibits the characteristics of a standard one-step growth curve and can efficiently replicate and express exogenous genes (A) The results of virus titer determination of HSV-1/WT, RG2001m, RG2002m, RG2005m, RG2011m, and RG2012m in Vero cells 48 h after infection. (B) Vero cells were infected with oHSV-1 at a multiplicity of infection (MOI) = 1, and the virus titers were determined at 0, 8, 16, 24, 32, 40, and 48 h, respectively, and a growth curve was drawn. (C) The results of virus titer determination of oHSV-1 in colon cancer cells (CT26, HCT116, and HT29) 48 h after infection. (D–F) The growth curves of oHSV-1 in colon cancer cells (CT26, HCT116, and HT29). (G) At MOI = 10, IL-15 expression levels in cell supernatants of HSV-1/WT, RG2001m, RG2005m, and RG2012m at 24, 48, and 72 h post-infection (mouse IL-15 ELISA Kit, elabscience). (H) At MOI = 10, IL-12 expression levels in cell supernatants of HSV-1/WT, RG2002m, RG2005m, and RG2012m at 24, 48, and 72 h post-infection (mouse IL-12 ELISA Kit, elabscience). (I) At MOI = 10, chemokine CCL5 expression levels in cell supernatants of HSV-1/WT, RG2011m, and RG2012m at 24, 48, and 72 h post-infection (mouse CCL5 ELISA Kit, elabscience). (Data are presented as mean ± SD. Comparisons between datasets were performed using one-way ANOVA and Student’s t test, with p values calculated [ n = 3]) ( p > 0.05, ns; p < 0.05, ∗; p < 0.01, ∗ ∗; p < 0.001, ∗ ∗ ∗).

Article Snippet: Cell Lines: Vero (African green monkey kidney, lab-preserved), murine CT26, and human HCT116/HT29 colorectal cancer cells (Wuhan Procell) were cultured in high-glucose DMEM with 10% FBS and antibiotics under standard mammalian conditions.

Techniques: Virus, Infection, Expressing, Enzyme-linked Immunosorbent Assay

Journal: iScience

Article Title: Triple-armed oncolytic HSV enhances antitumor immunity by remodeling the tumor microenvironment in subcutaneous murine CRC

doi: 10.1016/j.isci.2026.115883

Figure Lengend Snippet: Killing effect of recombinant oHSV-1 on colon cancer cells (A–C) CT26 (A), HCT116 (B), and HT29 (C) colon cancer cells were infected with recombinant oncolytic virus at multiplicity of infection (MOI) of 0.5, 1, and 5, respectively. The cell killing rate was detected by cell counting kit-8 (CCK8) assay 48 h after infection. The results showed that the killing effect of the virus on the three colon cancer cells was enhanced in an MOI - dependent manner. (D–F) CT26 (D), HCT116 (E), and HT29 (F) cells were infected with recombinant oncolytic virus at MOI = 1. The killing rate was measured by CCK8 assay at 24, 48, and 72 h after infection, suggesting that the killing effect of the virus on colon cancer cells was significantly enhanced with the prolongation of action time. (The values are presented as mean ± SD. The datasets were compared via one-way ANOVA. n = 3) ( p > 0.05, ns; p < 0.05, ∗; p < 0.01, ∗ ∗; p < 0.001, ∗ ∗ ∗.).

Article Snippet: Cell Lines: Vero (African green monkey kidney, lab-preserved), murine CT26, and human HCT116/HT29 colorectal cancer cells (Wuhan Procell) were cultured in high-glucose DMEM with 10% FBS and antibiotics under standard mammalian conditions.

Techniques: Recombinant, Infection, Virus, Cell Counting, CCK-8 Assay

Journal: iScience

Article Title: Triple-armed oncolytic HSV enhances antitumor immunity by remodeling the tumor microenvironment in subcutaneous murine CRC

doi: 10.1016/j.isci.2026.115883

Figure Lengend Snippet: Therapeutic effect of oHSV-1 on CT26 tumor-bearing mice (A) Schematic diagram of the experimental procedure: on day 0, 1×10 6 CT26 cells were suspended in 100 μL of PBS and subcutaneously injected into the right abdomen of immunocompetent Balb/c mice. From day 10, tumor-bearing mice with uniform tumor size were selected and treated with virus by intratumoral injection. Each mouse was injected with 2 × 10 7 PFU of virus (dissolved in 10 μL of PBS) each time, and the treatment was repeated every 3 days for a total of 4 times. When the tumor volume exceeded 2000 mm 3 , the mice were euthanized and counted as death events ( n = 13). (B) Dynamic changes in tumor volume in different treatment groups: The trends of tumor volume changes during the treatment in the PBS control group, HSV-1/WT group, RG2001m group, RG2002m group, RG2005m group, RG2011m group, and RG2012m group were shown respectively ( n = 8). (C) Mouse survival curves: The survival status of mice in the PBS control group, HSV-1/WT group, RG2001m group, RG2002m group, RG2005m group, RG2011m group, and RG2012m group was recorded until day 50, and survival curves were drawn ( n = 8). (D) Anatomical images of tumor tissues on day 21: five tumor-bearing mice were randomly selected and sacrificed in each group, and the gross morphology of the tumor tissues was photographed after dissection (Data are presented as mean ± SD. Comparisons between datasets were performed using one-way ANOVA and Student’s t test, as well as survival analysis, with p values calculated [ n = 5]). ( p > 0.05, ns; p < 0.05, ∗; p < 0.01, ∗ ∗; p < 0.001, ∗ ∗ ∗).

Article Snippet: Cell Lines: Vero (African green monkey kidney, lab-preserved), murine CT26, and human HCT116/HT29 colorectal cancer cells (Wuhan Procell) were cultured in high-glucose DMEM with 10% FBS and antibiotics under standard mammalian conditions.

Techniques: Injection, Virus, Control, Dissection

Journal: iScience

Article Title: Triple-armed oncolytic HSV enhances antitumor immunity by remodeling the tumor microenvironment in subcutaneous murine CRC

doi: 10.1016/j.isci.2026.115883

Figure Lengend Snippet: oHSV-1 exhibits the characteristics of a standard one-step growth curve and can efficiently replicate and express exogenous genes (A) The results of virus titer determination of HSV-1/WT, RG2001m, RG2002m, RG2005m, RG2011m, and RG2012m in Vero cells 48 h after infection. (B) Vero cells were infected with oHSV-1 at a multiplicity of infection (MOI) = 1, and the virus titers were determined at 0, 8, 16, 24, 32, 40, and 48 h, respectively, and a growth curve was drawn. (C) The results of virus titer determination of oHSV-1 in colon cancer cells (CT26, HCT116, and HT29) 48 h after infection. (D–F) The growth curves of oHSV-1 in colon cancer cells (CT26, HCT116, and HT29). (G) At MOI = 10, IL-15 expression levels in cell supernatants of HSV-1/WT, RG2001m, RG2005m, and RG2012m at 24, 48, and 72 h post-infection (mouse IL-15 ELISA Kit, elabscience). (H) At MOI = 10, IL-12 expression levels in cell supernatants of HSV-1/WT, RG2002m, RG2005m, and RG2012m at 24, 48, and 72 h post-infection (mouse IL-12 ELISA Kit, elabscience). (I) At MOI = 10, chemokine CCL5 expression levels in cell supernatants of HSV-1/WT, RG2011m, and RG2012m at 24, 48, and 72 h post-infection (mouse CCL5 ELISA Kit, elabscience). (Data are presented as mean ± SD. Comparisons between datasets were performed using one-way ANOVA and Student’s t test, with p values calculated [ n = 3]) ( p > 0.05, ns; p < 0.05, ∗; p < 0.01, ∗ ∗; p < 0.001, ∗ ∗ ∗).

Article Snippet: CT26 , Wuhan Procell Life Science & Technology Co., Ltd., China , Cat. No. CL-0071; RRID:CVCL_7256.

Techniques: Virus, Infection, Expressing, Enzyme-linked Immunosorbent Assay

Journal: iScience

Article Title: Triple-armed oncolytic HSV enhances antitumor immunity by remodeling the tumor microenvironment in subcutaneous murine CRC

doi: 10.1016/j.isci.2026.115883

Figure Lengend Snippet: Killing effect of recombinant oHSV-1 on colon cancer cells (A–C) CT26 (A), HCT116 (B), and HT29 (C) colon cancer cells were infected with recombinant oncolytic virus at multiplicity of infection (MOI) of 0.5, 1, and 5, respectively. The cell killing rate was detected by cell counting kit-8 (CCK8) assay 48 h after infection. The results showed that the killing effect of the virus on the three colon cancer cells was enhanced in an MOI - dependent manner. (D–F) CT26 (D), HCT116 (E), and HT29 (F) cells were infected with recombinant oncolytic virus at MOI = 1. The killing rate was measured by CCK8 assay at 24, 48, and 72 h after infection, suggesting that the killing effect of the virus on colon cancer cells was significantly enhanced with the prolongation of action time. (The values are presented as mean ± SD. The datasets were compared via one-way ANOVA. n = 3) ( p > 0.05, ns; p < 0.05, ∗; p < 0.01, ∗ ∗; p < 0.001, ∗ ∗ ∗.).

Article Snippet: CT26 , Wuhan Procell Life Science & Technology Co., Ltd., China , Cat. No. CL-0071; RRID:CVCL_7256.

Techniques: Recombinant, Infection, Virus, Cell Counting, CCK-8 Assay

Journal: iScience

Article Title: Triple-armed oncolytic HSV enhances antitumor immunity by remodeling the tumor microenvironment in subcutaneous murine CRC

doi: 10.1016/j.isci.2026.115883

Figure Lengend Snippet: Therapeutic effect of oHSV-1 on CT26 tumor-bearing mice (A) Schematic diagram of the experimental procedure: on day 0, 1×10 6 CT26 cells were suspended in 100 μL of PBS and subcutaneously injected into the right abdomen of immunocompetent Balb/c mice. From day 10, tumor-bearing mice with uniform tumor size were selected and treated with virus by intratumoral injection. Each mouse was injected with 2 × 10 7 PFU of virus (dissolved in 10 μL of PBS) each time, and the treatment was repeated every 3 days for a total of 4 times. When the tumor volume exceeded 2000 mm 3 , the mice were euthanized and counted as death events ( n = 13). (B) Dynamic changes in tumor volume in different treatment groups: The trends of tumor volume changes during the treatment in the PBS control group, HSV-1/WT group, RG2001m group, RG2002m group, RG2005m group, RG2011m group, and RG2012m group were shown respectively ( n = 8). (C) Mouse survival curves: The survival status of mice in the PBS control group, HSV-1/WT group, RG2001m group, RG2002m group, RG2005m group, RG2011m group, and RG2012m group was recorded until day 50, and survival curves were drawn ( n = 8). (D) Anatomical images of tumor tissues on day 21: five tumor-bearing mice were randomly selected and sacrificed in each group, and the gross morphology of the tumor tissues was photographed after dissection (Data are presented as mean ± SD. Comparisons between datasets were performed using one-way ANOVA and Student’s t test, as well as survival analysis, with p values calculated [ n = 5]). ( p > 0.05, ns; p < 0.05, ∗; p < 0.01, ∗ ∗; p < 0.001, ∗ ∗ ∗).

Article Snippet: CT26 , Wuhan Procell Life Science & Technology Co., Ltd., China , Cat. No. CL-0071; RRID:CVCL_7256.

Techniques: Injection, Virus, Control, Dissection

Journal: Frontiers in Immunology

Article Title: STAT6 inhibition of M2 macrophages suppresses tumor growth by modulating the tumor microenvironment in colon cancer model

doi: 10.3389/fimmu.2026.1733991

Figure Lengend Snippet: TAMpep-IP suppresses tumor growth in the colon cancer model. (A) BALB/c mice were subcutaneously inoculated with CT26 colon carcinoma cells (3 × 10 5 cells per mouse). Starting on day 7 post-inoculation, TAMpep-IP (400 nmol/kg) was administered subcutaneously every three days for a total of seven doses. (B) Representative images of tumors excised at the experimental endpoint (day 25) showed visibly reduced tumor size in the TAMpep-IP–treated group compared to control. (C) Tumor volumes were measured every 3 days following tumor implantation. Mice treated with TAMpep-IP exhibited significantly reduced tumor growth relative to the control group (control: n = 6; TAMpep-IP: n = 6). (D) Tumor proliferation was evaluated by immunohistochemical staining of Ki-67 in tumor sections. Quantitative analysis showed a significantly lower proportion of Ki-67 + proliferating cells in TAMpep-IP–treated tumors. Representative immunohistochemistry images were acquired at ×100 magnification. Scale bar = 1000 μm. All data are presented as mean ± SEM. *p<0.05, ***p<0.001.

Article Snippet: The murine colon carcinoma cell line CT26 (KCLB 80009; Korean Cell Line Bank, Seoul, Korea) was cultured in Dulbecco’s modified Eagle’s medium (DMEM) (D5671; Welgene, Gyeongsangbuk, Korea) supplemented with 10% heat-inactivated FBS, 100 U/mL penicillin, and 1% penicillin–streptomycin.

Techniques: Control, Tumor Implantation, Immunohistochemical staining, Staining, Immunohistochemistry

Journal: Frontiers in Immunology

Article Title: STAT6 inhibition of M2 macrophages suppresses tumor growth by modulating the tumor microenvironment in colon cancer model

doi: 10.3389/fimmu.2026.1733991

Figure Lengend Snippet: TAMpep-IP reduces M2 macrophages in tumor tissues of colon cancer model. (A) Tumor-infiltrating immune cells were isolated from CT26 tumors in control and TAMpep-IP–treated mice. Flow cytometry was used to identify CD206 + F4/80 + macrophages within the CD45 + CD11b + population. TAMpep-IP significantly decreased the proportion of M2-like tumor-associated macrophages. (B) Quantitative RT-PCR analysis of tumor tissues revealed that TGF-β mRNA expression, a key M2-associated cytokine, was significantly reduced in TAMpep-IP–treated tumors compared to controls. (C) Western blot analysis of tumor showed a marked decrease in CD206 protein levels following TAMpep-IP, indicating effective suppression of M2 macrophage markers. (D) CD206 + macrophages were further visualized by immunohistochemical staining of tumor sections. ImageJ-based quantification confirmed a significant reduction in CD206 + area in TAMpep-IP–treated tumors. Representative immunohistochemistry images were acquired at ×100 magnification. Scale bar = 1000 μm. All data are presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001.

Article Snippet: The murine colon carcinoma cell line CT26 (KCLB 80009; Korean Cell Line Bank, Seoul, Korea) was cultured in Dulbecco’s modified Eagle’s medium (DMEM) (D5671; Welgene, Gyeongsangbuk, Korea) supplemented with 10% heat-inactivated FBS, 100 U/mL penicillin, and 1% penicillin–streptomycin.

Techniques: Isolation, Control, Flow Cytometry, Quantitative RT-PCR, Expressing, Western Blot, Immunohistochemical staining, Staining, Immunohistochemistry

Journal: Frontiers in Immunology

Article Title: STAT6 inhibition of M2 macrophages suppresses tumor growth by modulating the tumor microenvironment in colon cancer model

doi: 10.3389/fimmu.2026.1733991

Figure Lengend Snippet: TAMpep-IP enhances inflammatory cytokine expression and activated CD8 + T cells in tumor tissues of colon cancer model. (A) Flow cytometry was used to evaluate CD8 + T cell function in CT26 tumor tissues from control and TAMpep-IP-treated mice. TAMpep-IP significantly increased the proportion of activated Granzyme B + CD8 + T cells, while reducing the frequency of exhausted Tim-3 + CD8 + T cells, indicating enhanced cytotoxic T cell activity. (B, C) Confocal immunofluorescence analysis was performed on tumor sections stained with DAPI (nuclei), anti-CD8 (green), anti-Granzyme B (red), and anti-PD-1 (red). Activated CD8 + T cells were identified by co-localization of CD8 and Granzyme B, whereas exhausted CD8 + T cells were identified by co-localization of CD8 and PD-1. Quantification revealed a significant increase in intertumoral CD8 + Granzyme B + T cells and a concomitant decrease in CD8 + PD-1 + exhausted T cells following TAMpep-IP. Representative confocal images were acquired using a 40× objective lens. Scale bar = 20 μm. (D) Quantitative RT-PCR analysis of CT26 tumor tissues showed significantly elevated mRNA levels of pro-inflammatory cytokines TNF-α, IL-1β, and IL-12 in TAMpep-IP–treated mice compared to controls, indicating induction of a pro-inflammatory tumor microenvironment. All data are presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001, ****p < 0.0001.

Article Snippet: The murine colon carcinoma cell line CT26 (KCLB 80009; Korean Cell Line Bank, Seoul, Korea) was cultured in Dulbecco’s modified Eagle’s medium (DMEM) (D5671; Welgene, Gyeongsangbuk, Korea) supplemented with 10% heat-inactivated FBS, 100 U/mL penicillin, and 1% penicillin–streptomycin.

Techniques: Expressing, Flow Cytometry, Cell Function Assay, Control, Activity Assay, Immunofluorescence, Staining, Quantitative RT-PCR

Journal: iScience

Article Title: A fully human pan VL9 HLA-E TCRm antibody enables functional dissection of HLA-E biology and checkpoint signaling

doi: 10.1016/j.isci.2026.115669

Figure Lengend Snippet: Combination therapy with ABX002 surrogate and anti-PD-(L)1 antibodies enhances therapeutic efficacy in a mouse colorectal tumor model (A) Schematic representation illustrating that MHC class I SPs required for CD94/NKG2A engagement are presented on the cell surface only following inflammatory stimulation. (B) Experimental schematic of the CT26 tumor model and treatment strategy. (C) Mean tumor growth curves in mice treated with monotherapy (ABX002 surrogate or anti-PD-L1) or combination therapy. (D) Kaplan-Meier survival curves for each treatment group, with the number of surviving mice indicated alongside the survival plot ( n = 15 per group; anti PD-L1 group n = 9). Individual tumor growth curves for each group are shown in . (E) Tumor growth comparison between mice previously treated with the ABX002 surrogate and rechallenged with CT26 or 4T1 tumor cells ( n = 3), versus naive mice newly engrafted with CT26 or 4T1 tumor cells ( n = 4). Triangle markers denote the day of tumor engraftment. (F) Flow cytometric analysis of tumor samples from control-treated mice. Tumors were stained ex vivo using ABX002 surrogate (blue) and anti Qa-1 b (clone 6A8; pink) to detect Qa-1 b heavy chain and Qdm/Qa-1 b complexes, respectively. Background-subtracted gMFI values were calculated by removing signal from isotype control stained samples. Error bars represent mean ± SD. See also .

Article Snippet: CT26 , ATCC , Cat#CRL-2638; RIID:CVCL_7254.

Techniques: Drug discovery, Comparison, Control, Staining, Ex Vivo