期刊
PLOS PATHOGENS
卷 17, 期 10, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.ppat.1009693
关键词
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资金
- NIH [RO1AI143790]
This study demonstrates the involvement of IL-17A-producing ILCs in microbiota-driven immunopathology in cutaneous leishmaniasis. Skin microbiota promotes the generation of ROR gamma t(+) IL-17A-producing ILCs, which exacerbate skin inflammation in the disease.
Innate lymphoid cells (ILCs) comprise a heterogeneous population of immune cells that maintain barrier function and can initiate a protective or pathological immune response upon infection. Here we show the involvement of IL-17A-producing ILCs in microbiota-driven immunopathology in cutaneous leishmaniasis. IL-17A-producing ILCs were ROR gamma t(+) and were enriched in Leishmania major infected skin, and topical colonization with Staphylococcus epidermidis before L. major infection exacerbated the skin inflammatory responses and IL-17A-producing ROR gamma t(+) ILC accumulation without impacting type 1 immune responses. IL-17A responses in ILCs were directed by Batf3 dependent CD103(+) dendritic cells and IL-23. Moreover, experiments using Rag1(-/-) mice established that IL-17A(+) ILCs were sufficient in driving the inflammatory responses as depletion of ILCs or neutralization of IL-17A diminished the microbiota mediated immunopathology. Taken together, this study indicates that the skin microbiota promotes ROR gamma t(+) IL-17A-producing ILCs, which augment the skin inflammation in cutaneous leishmaniasis.
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