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Image Search Results
Journal: Journal of immunology (Baltimore, Md. : 1950)
Article Title: Proinflammatory effects of TWEAK/Fn14 interactions in glomerular mesangial cells.
doi: 10.4049/jimmunol.176.3.1889
Figure Lengend Snippet: FIGURE 7. Abs to IL-1 or IL-6 do not inhibit chemokine secretion in response to TWEAK. C57BL/6 mesangial cells were stimulated for 24 h with and without 100 ng/ml TWEAK and 5 g/ml monoclonal rat anti- mouse IL-1 and IL-6. Rat IgG is an IgG2b mAb that was the rat isotype- matched control. A, CCL2/MCP-1; B, CCL5/RANTES; C, CXCL1/KC. Shown here are the mean SD values for duplicate wells; similar results were found in several independent experiments.
Article Snippet: We found that there was significant binding to the surface of murine mesangial cells by hFc-TWEAK (Fig. 1B), but not by a CTLA4-Ig control fusion protein (R&D Systems) or a
Techniques: Control
Journal: Journal of immunology (Baltimore, Md. : 1950)
Article Title: Proinflammatory effects of TWEAK/Fn14 interactions in glomerular mesangial cells.
doi: 10.4049/jimmunol.176.3.1889
Figure Lengend Snippet: FIGURE 9. Murine anti-TWEAK mAbs prevent the induction of che- mokines in response to TWEAK stimulation of mesangial cells. The 2.P5.G9 and 2P2.D10 are two IgG2a mouse mAbs against murine TWEAK, derived by immunization of TWEAK knockout mice, as de- scribed in Materials and Methods. P1.17 is an isotype-matched control Ab. C57BL/6 mesangial cells were left untreated, or treated with TWEAK with and without these mAbs at a concentration of 5 g/ml for 24 h. Shown here are the mean SD values for duplicate wells; similar results were found in several independent experiments.
Article Snippet: We found that there was significant binding to the surface of murine mesangial cells by hFc-TWEAK (Fig. 1B), but not by a CTLA4-Ig control fusion protein (R&D Systems) or a
Techniques: Derivative Assay, Knock-Out, Control, Concentration Assay
Journal: Scientific Reports
Article Title: In vitro complement activation via nucleocapsid and spike proteins of SARS-CoV-2 in COVID-19 patients
doi: 10.1038/s41598-025-20926-6
Figure Lengend Snippet: Comparison of the in vitro C3b and C4b complement depositions via spike (C3b(S) and C4b(S)) or nucleocapsid (C3b(N) and C4b(N)) recombinant proteins between patients with (Ab(+)) or without (Ab(-)) SARS-CoV-2-specific IgM and IgG antibodies from four different COVID-19 groups (CONV, HOSP, HOSP + O 2 and ICU). The in vitro C3b and C4b complement depositions were measured by our in-house complement deposition assays, where we used carrier free recombinant nucleocapsid or spike proteins and non-heat-inactivated patient sera. The p values for the pair-wise group comparisons on the violin plots were calculated by the Mann-Whitney tests. P values of significant differences are marked as p MW between without and with specific antibodies. Non-significant differences are marked as n.s.
Article Snippet:
Techniques: Comparison, In Vitro, Recombinant, MANN-WHITNEY
Journal: Scientific Reports
Article Title: In vitro complement activation via nucleocapsid and spike proteins of SARS-CoV-2 in COVID-19 patients
doi: 10.1038/s41598-025-20926-6
Figure Lengend Snippet: Comparison of the levels of SARS-CoV-2-specific IgM and IgG among four COVID-19 groups (CONV, HOSP, HOSP + O2, ICU) measured by Generic Assays CoV-2 IgM or IgG ( a ). The percentages of SARS-CoV-2-specific IgG or IgM positivity were shown also for four different COVID-19 groups. The numbers represent the mean percentages of SARS-CoV-2-specific IgM in blue or specific IgG in green circle sectors ( b ). The levels of total S- or N-specific IgG were quantified by in-house ELISA, normalized to positive and negative serum samples ( c ). The levels of S-specific and N-specific IgG1 ( d ) and IgG3 ( e ) subclasses were quantified by in-house ELISA calibrated with purified human IgG1 and IgG3. The p -values ( p KW ) were determined by Kruskal-Wallis test.
Article Snippet:
Techniques: Comparison, Enzyme-linked Immunosorbent Assay, Purification
Journal: Scientific Reports
Article Title: In vitro complement activation via nucleocapsid and spike proteins of SARS-CoV-2 in COVID-19 patients
doi: 10.1038/s41598-025-20926-6
Figure Lengend Snippet: The in vitro C3b and C4b complement depositions via spike (C3b(S) and C4b(S)) recombinant protein are plotted by the levels of S-specific IgG1 and IgG3 in CONV individuals and in the other three hospitalized COVID-19 groups (HOSP, HOSP + O 2 and ICU) ( a ). The in vitro C3b and C4b complement depositions via nucleocapsid (C3b(N) and C4b(N)) recombinant protein are plotted by the levels of N-specific IgG1 and IgG3 in CONV individuals and in the other three hospitalized COVID-19 groups (HOSP, HOSP + O 2 and ICU) ( b ).
Article Snippet:
Techniques: In Vitro, Recombinant
Journal: Scientific Reports
Article Title: In vitro complement activation via nucleocapsid and spike proteins of SARS-CoV-2 in COVID-19 patients
doi: 10.1038/s41598-025-20926-6
Figure Lengend Snippet: Comparison of the levels of SARS-CoV-2-specific IgM and IgG antibodies, and in vivo complement profiles in all COVID-19 patients between low and high in vitro C3b(N) complement depositions. The p values for the pair-wise group comparisons on the violin plots were calculated by the Mann-Whitney tests. Asterisks indicate p value < 0.0143 , considered significant results after 5% FDR correction using the Benjamini-Hochberg method.
Article Snippet:
Techniques: Comparison, In Vivo, In Vitro, MANN-WHITNEY
Journal: PLOS ONE
Article Title: Crystalline silica-exposed human lung epithelial cells presented enhanced anchorage-independent growth with upregulated expression of BRD4 and EZH2 in autocrine and paracrine manners
doi: 10.1371/journal.pone.0285354
Figure Lengend Snippet: (A) ELISA of EGF, TNF-α, IL-6, and TGF-β1 was performed with the culture supernatants of nonadherent NL20, BEAS-2B, and 16HBE 4–6 days after incubation with autocrine CS or BPDE CM compared with the autocrine control CM. ELISA of EGF, TNF-α, and IL-6 was also conducted with the culture supernatants 48 h after exposure to CS in adherent bronchial cell lines. Asterisks indicate a significant difference in concentration (*p < 0.05, **p < 0.01). Relative values are shown as mean ± SD from three independent experiments. (B) Anchorage-independent growth of NL20, BEAS-2B, and 16HBE cells was measured using MTT 5–6 days after the administration of recombinant human EGF, TNF-α, and IL-6. The MTT assay was performed for autocrine CS CM-incubated nonadherent NL20 and BEAS-2B cells four and five days after EGF-neutralizing antibody (NtAb) treatment, respectively, and for autocrine CS CM-incubated nonadherent 16HBE cells, five days after TNF-α NtAb treatment. The MTT assay was also performed for autocrine CS CM-incubated nonadherent bronchial cell lines five days after IL-6 NtAb administration. Asterisks indicate a significant difference in growth (*p < 0.05, **p < 0.01). Relative values are shown as mean ± SD from three independent experiments. (C) Expression of BRD4 and EZH2 in nonadherent 16HBE cells three days after the administration of recombinant human TNF-α determined using western blotting and the expression of BRD4 and EZH2 3–4 days after treatment of nonadherent NL20 and BEAS-2B cells with recombinant human EGF.
Article Snippet: Mouse anti-human EGF neutralizing antibody (NtAb), goat anti-human TNF-α NtAb, and
Techniques: Enzyme-linked Immunosorbent Assay, Incubation, Control, Concentration Assay, Recombinant, MTT Assay, Expressing, Western Blot
Journal: Bioengineering & Translational Medicine
Article Title: Disease modifying biomaterials for modulating mechanical allodynia in a preclinical model of rheumatoid arthritis
doi: 10.1002/btm2.70054
Figure Lengend Snippet: Therapeutic evaluation of ATRA‐PLGA MP in early‐stage arthritis in SKG mice. (a) Study design: Arthritis was induced in SKG mice via IP injection of mannan on day 0. Mice received daily IP injections of CTLA‐4‐Ig (10 mg × kg −1 ), IgG (10 mg × kg −1 ), or vehicle (1 x PBS) from day 0 to day 2. On day 3, mice were administered IA either Blank‐PLGA MP (control) or ATRA‐PLGA MP. (b) Mice were divided into four experimental treatment groups. Clinical arthritis scores in female (c) and male (e) mice, including an inset showing the AUC analysis of scores throughout the study. Mechanical allodynia in female (d) and male (f) mice, assessed via von Frey testing with corresponding AUC analysis. Clinical score and mechanical allodynia data are shown as mean ± SEM ( n > 5), while AUC data are presented as mean ± SD. For panels (c) and (e), the baseline for AUC was set to 0, while for panels (d) and (f), the baseline was defined as the group average on day 0. Statistical analysis was performed using one‐way ANOVA.
Article Snippet:
Techniques: Injection, Control