期刊
PLOS ONE
卷 10, 期 5, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0128335
关键词
-
资金
- [NIHR01AI-110201]
Intestinal infection with the intracellular parasite Toxoplasma gondii results in the translocation of commensal bacteria to peripheral organs and the development of a T cell response specific to the microbiota. In naive mice, the recently described ROR gamma t(+) group 3 innate lymphoid cell (ILC) population plays a critical role in promoting intestinal barrier function and limiting responses to gut-resident commensal bacteria. Given this role for group 3 ILCs, studies were performed to evaluate whether these cells might influence the immune response to mucosal infection with T. gondii. Phenotypic characterization of ROR gamma t(+) ILCs in T. gondii infected mice revealed that this population decreased following challenge but the population that remained expressed costimulatory molecules and IL-22. One factor that influences the maintenance of ROR gamma t(+) ILCs is the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor, and Ahr(-/-) mice have a marked defect in the lamina propria group 3 ILC population. When Ahr(-/-) mice were challenged with T. gondii, they lost more weight than wild type controls. This disease course in Ahr(-/-) animals was associated with increased T cell responses to Toxoplasma antigen and crude commensal antigen preparations. Together, these data suggest that group 3 ILCs have a role in limiting T cell activation during intestinal infection.
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