Intestinal IL-17R Signaling Controls Secretory IgA and Oxidase Balance in Citrobacter rodentium Infection

被引:12
作者
Matsunaga, Yasuka [1 ]
Clark, Trevon [1 ]
Wanek, Alanna G. [1 ]
Bitoun, Jacob P. [2 ]
Gong, Qingqing [3 ]
Good, Misty [3 ]
Kolls, Jay K. [1 ]
机构
[1] Tulane Sch Med, Ctr Translat Res Infect & Inflammat, New Orleans, LA 70112 USA
[2] Tulane Sch Med, Dept Microbiol & Immunol, New Orleans, LA 70112 USA
[3] Washington Univ, Dept Pediat, St Louis, MO 63110 USA
关键词
MUCOSAL IMMUNITY; HOST PROTECTION; HELPER-CELLS; INNATE; MICROBIOTA; BACTERIA; RECEPTOR; EPITHELIUM; RESPONSES; DEFENSE;
D O I
10.4049/jimmunol.2000591
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Type 17 cytokines have been strongly implicated in mucosal immunity, in part by regulating the production of antimicrobial peptides. Using a mouse model of Citrobacter rodentium infection, which causes colitis, we found that intestinal IL-17RA and IL-17RC were partially required for control of infection in the colon and IL-17 regulates the production of luminal hydrogen peroxide as well as expression of Tnsf13. Reduced Tnfsf13 expression was associated with a profound defect in generating C. rodentium-specific IgA(+) Ab-secreting cells. Taken together, intestinal IL-17R signaling plays key roles in controlling invading pathogens, in part by regulating luminal hydrogen peroxide as well as regulating the generation of pathogen-specific IgA(+) Ab-secreting cells.
引用
收藏
页码:766 / 775
页数:10
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