Journal
JOURNAL OF IMMUNOLOGY
Volume 183, Issue 3, Pages 2037-2044Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0802918
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Funding
- National Institutes of Health [A172943, A161570, A1074878, A142334, A141158]
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IL-27 limits CD4(+) T(H)17 cell development in vitro and during inflammatory responses in the CNS. However, whether IL-27-IL-7R interactions regulate the homeostasis or function of CD4(+) T cell populations in the intestine is unknown. To test this, we examined CD4(+) T cell populations in the intestine of wild-type and IL-27R(-/-) mice. Naive IL-27R(-/-) mice exhibited a selective decrease in the frequency of IFN-gamma producing CD4(+) T(H)1 cells and an increase in the frequency of T(H)17 cells in gut-associated lymphoid tissues. Associated with elevated expression of IL-17A, IL-27R(-/-) mice exhibited earlier onset and significantly increased severity of clinical disease compared with wild-type controls in a murine model of intestinal inflammation. Rag(-/-)IL-27R(-/-) mice were also more susceptible than Rag(-/-) mice to development of dextran sodium sulfate-induced intestinal inflammation, indicating an additional role for IL-27-IL-27R in the regulation of innate immune cell function. Consistent with this, IL-27 inhibited proinflammatory cytokine production by activated neutrophils. Collectively, these data identify a role for IL-27-IL-27R interaction in controlling the homeostasis of the intestinal T cell pool and in limiting intestinal inflammation through regulation of innate and adaptive immune cell function. The Journal of Immunology, 2009, 183: 2037-2044.
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