IL-17 plays differential role in primary verse memory immune responses and recognition of cellular verse soluble antigens (87.30)

Abstract

Abstract IL-17 is a proinflammatory cytokine that has been linked to many autoimmune related diseases such as rheumatoid arthritis, asthma, lupus, and multiple sclerosis. Recent studies have indicated that IL-17 may also play central role in driving the development of germinal center-derived autoantibody and Th response in an autoimmune disease model setting. In addition, activated and memory T cells can both produce IL-17. In this report, we found that IL-17 differentially affected primary versus memory immune response to cellular versus soluble antigen. Briefly, we initiated primary or memory immune response with SRBC or OVA and blocked IL-17 using anti-IL-17 antibody (Amgen). We found that blockade of IL-17 did not affect OVA-induced primary or memory response, nor did it affect SRBC-induced memory response; however, the blockade inhibited SRBC-induced primary response. SRBC-induced hemagglutination, DTH and specific T cell proliferation were inhibited; serum IFN-gamma, IL-12 and SRBC-specific IgG1 were decreased; numbers of germinal centers and IgG1-producing B cells in the germinal center were decreased; IL-17R knockout-CD4 T cells showed a decreased expression of BTLA and ICOS; however, percentages of CD4, CD8, CD3 and CD19 subsets in the spleen did not change with the antibody blockade. Our report suggests a differential role of IL-17 on T-B, T-DC cell interaction or Ig class switch in response to cellular versus soluble antigens, and primary versus memory immune response.