Journal
SCIENCE
Volume 366, Issue 6464, Pages 445-+Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aax6624
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Funding
- Intramural Research Program of NIAID, NIH [ZIA-AI001115, ZIA-AI001132]
- NIH Extramural Research Program [U19-AI111143, R01-DK110174, DP1-DK113598, DP2-AI144968]
- Cancer Research Institute Irvington Postdoctoral Fellowship Program
- European Molecular Biology Organization (EMBO) Long-Term Fellowship Program
- ARC Foundation
- National Institute of General Medical Sciences (NIGMS) Postdoctoral Research Associate Training (PRAT) Program
- Howard Hughes Medical Institute (HHMI) Hanna H. Gray Fellows Program
- HHMI-Simons Faculty Scholars Program
- Chan Zuckerberg Biohub
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [ZIAAI001115, ZIAAI001132] Funding Source: NIH RePORTER
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How early-life colonization and subsequent exposure to the microbiota affect long-term tissue immunity remains poorly understood. Here, we show that the development of mucosal-associated invariant T (MAIT) cells relies on a specific temporal window, after which MAIT cell development is permanently impaired. This imprinting depends on early-life exposure to defined microbes that synthesize riboflavin-derived antigens. In adults, cutaneous MAIT cells are a dominant population of interleukin-17A (IL-17A)-producing lymphocytes, which display a distinct transcriptional signature and can subsequently respond to skin commensals in an IL-1-, IL-18-, and antigen-dependent manner. Consequently, local activation of cutaneous MAIT cells promotes wound healing. Together, our work uncovers a privileged interaction between defined members of the microbiota and MAIT cells, which sequentially controls both tissue-imprinting and subsequent responses to injury.
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