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- W4313360107 abstract "Abstract Background Pro-inflammatory T helper (Th)17 or Th1 cell responses (IL17, IFNγ, TNFα) drive autoimmune pathology in rheumatoid arthritis (RA) at the expense of anti-inflammatory/regulatory (IL4, IL10, TGFβ) T cell responses. Ligand Epitope Antigen Presenting System (LEAPS) vaccines, composed of cell-binding and immunodominant peptides, can down-modulate Th17 or Th1 activity and thus have the potential to treat ongoing RA. Choice of appropriate treatment requires knowledge of key cytokines driving disease as well as responses to therapy. Experimental design Serum cytokines were assayed in mouse models of RA including proteoglycan-induced arthritis (PGIA) recombinant proteoglycan G1 domain-induced arthritis (GIA) and collagen-induced arthritis (CIA) after arthritic mice had been treated with LEAPS vaccines. Serum cytokine levels and ratios of anti-inflammatory to pro-inflammatory cytokines were correlated with visual and histopathologic scores of disease. Results Serum levels of pro-inflammatory cytokines were elevated in control mice with either PGIA, GIA, or CIA. Reduced disease progression in mice treated with LEAPS vaccines was accompanied by decreased pro-inflammatory cytokine levels and increased ratios of anti-inflammmatory/regulatory to pro-inflammatory cytokines. Conclusion Serum concentrations and ratios of key disease-related cytokines can predict therapeutic efficacy in different animal models of RA. Successful vaccine therapy is associated with ratios shifted in favor of anti-inflammatory/regulatory cytokines. The ability to predict cytokine responses to therapy will allow better design or choice of appropriate immunomodulatory LEAPS vaccines and other therapies in RA." @default.
- W4313360107 created "2023-01-06" @default.
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- W4313360107 date "2017-05-01" @default.
- W4313360107 modified "2023-09-25" @default.
- W4313360107 title "Key serum cytokine markers for evaluating the efficacy of vaccine therapy in autoimmune models of rheumatoid arthritis" @default.
- W4313360107 doi "https://doi.org/10.4049/jimmunol.198.supp.224.14" @default.
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