期刊
CELL HOST & MICROBE
卷 25, 期 6, 页码 777-+出版社
CELL PRESS
DOI: 10.1016/j.chom.2019.04.004
关键词
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资金
- NIH [R01 DK070855, T32 AI007520, F32 DK100074, T32 AI005284]
- Burroughs Wellcome Foundation Investigators in the pathogenesis of Infectious Diseases Award
- Welch Foundation [I-1874]
- Walter M. and Helen D. Bader Center for Research on Arthritis and Autoimmune Diseases
- Howard Hughes Medical Institute
- Gruss-Lipper postdoctoral fellowship
- Korean Health Technology R&D Project, Ministry of Health and Welfare, Republic of Korea [HI15C1095]
- Intramural Research Program of the National Cancer Institute
- Intramural Research Programs of the National Cancer Institute, National Institute of Arthritis and Musculoskeletal and Skin Diseases
- Intramural Research Programs of the National Human Genome Research Institute
- Dermatology Foundation Career Development Award
- UT Southwestern Disease Oriented Clinical Scholars Program
- Burroughs Wellcome Fund Career Award for Medical Scientists
- Burroughs Wellcome Fund Postdoctoral Enrichment Program Award
- NATIONAL CANCER INSTITUTE [ZIABC010938, ZIABC011558] Funding Source: NIH RePORTER
- NATIONAL HUMAN GENOME RESEARCH INSTITUTE [ZIAHG000180] Funding Source: NIH RePORTER
Vitamin A deficiency increases susceptibility to skin infection. However, the mechanisms by which vitamin A regulates skin immunity remain unclear. Here, we show that resistin-like molecule alpha (RELM alpha), a small secreted cysteine-rich protein, is expressed by epidermal keratinocytes and sebocytes and serves as an antimicrobial protein that is required for vitamin-A-dependent resistance to skin infection. RELM alpha was induced by microbiota colonization of the murine skin, was bactericidal in vitro, and was protected against bacterial infection of the skin in vivo. RELM alpha expression required dietary vitamin A and was induced by the therapeutic vitamin A analog isotretinoin, which protected against skin infection in a RELM alpha-dependent manner. The RELM family member Resistin was expressed in human skin, was induced by vitamin A analogs, and killed skin bacteria, indicating a conserved function for RELM proteins in skin innate immunity. Our findings provide insight into how vitamin A promotes resistance to skin infection.
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