4.6 Article

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

Journal

JOURNAL OF IMMUNOLOGY
Volume 206, Issue 4, Pages 766-775

Publisher

AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.2000591

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Funding

  1. National Institute of Diabetes and Digestive and Kidney Diseases [P30DK052574]
  2. Louisiana Board of Regents Endowed Chairs for Eminent Scholars program
  3. National Heart, Lung, and Blood Institute
  4. Public Health Service [R35HL139930]

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Type 17 cytokines, particularly IL-17, play crucial roles in mucosal immunity by regulating the production of antimicrobial peptides and controlling the generation of pathogen-specific IgA(+) antibody-secreting cells in the intestine.
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.

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