IL-17 promotes intestinal IgA response to intestinal infection but does not affect memory B cell development

• Published in: The Journal of immunology (1950) 2017-05, Vol.198 (1_Supplement), p.200-200.16
• Main Authors: Huang, Xiangsheng, Sun, Mingming, Chen, Feidi, Xiao, Yi, Chen, Liang, Yao, Suxia, Cong, Yingzi
• Format: Article
• Language: English
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.198.Supp.200.16

Secretory IgA is the principal immunoglobulin found in intestinal track and plays a crucial role in maintanence of intestinal homeostasis. We have previously demonstrated that Th17 cells, which produce IL-17, IL-21 and IL-22, promoted intestinal IgA responses to microbiota. However, the mechanisms involved are still largely unknown. In current study, we investigated the roles of Th17 cells in regulation of intestinal IgA response to enteric pathogen infection. We showed that adoptive transfer of CBir1-specific Th17 cells, which are specific for immunodominant gut bacterial antigen CBir1 flagellin, promoted intestinal IgA in T cell-deficient TCRβxδ−/− mice, which is inhibited by the blockade of IL-17 and IL-21. To determine whether IL-17 regulates memory IgA B cell responses to intestinal infection, we infect wild type (WT) and IL-17R−/− mice with Citrobacter Rodentium, and C. Rodentium in the intestines, as well as fecal C. Rodentium-specific IgA and lamina propria IgA+ memory B cells were assessed. IL-17R−/− mice shows less efficiency in C. Rodentium clearance, in that while there were almost no bacteria at week 2 after infection in WT mice, significant amounts of C. Rodentium were still present in IL-17R−/− mice. Consistently, in IL-17R−/− mice C. Rodentium-specific intestinal IgA production was impaired compare with WT mice, and the memory IgA development was diminished after re-infection. However, there was no difference in lamina propria IgA+ memory B cells between WT and IL-17R−/− mice. Collectively, our data demonstrated that the IL-17 promotes intestinal IgA responses to intestinal infection, however, it does not affect memory IgA B cell development.