期刊
SCIENCE TRANSLATIONAL MEDICINE
卷 5, 期 170, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scitranslmed.3005374
关键词
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资金
- NIH [AI061570, AI087990, AI074878, AI083480, AI095466, AI095608, AI102942, AI097333]
- Burroughs Wellcome Fund Investigator in Pathogenesis of Infectious Disease Award
- Swiss National Science Foundation Prospective Research Fellowship
- National Cancer Institute Comprehensive Cancer Center Support Grant [2-P30 CA016520]
- NIH/National Institute of Diabetes and Digestive and Kidney P30 Center for Molecular Studies in Digestive and Liver Diseases [P30-DK050306]
- Joint CHOP-Penn Center in Digestive, Liver and Pancreatic Medicine
- National Center for Research Resources, NIH
- National Center for Advancing Translational Sciences, NIH [KL2TR000139]
- Skin Disease Research Center, NIH [SDRC 5-P30-AR-057217]
- [KL2-RR024132]
- [AI085828]
- [T32-AI007532]
- [DP5OD012116]
Innate lymphoid cells (ILCs) are a recently identified family of heterogeneous immune cells that can be divided into three groups based on their differential developmental requirements and expression of effector cytokines. Among these, group 2 ILCs produce the type 2 cytokines interleukin-5 (IL-5) and IL-13 and promote type 2 inflammation in the lung and intestine. However, whether group 2 ILCs reside in the skin and contribute to skin inflammation has not been characterized. We identify a population of skin-resident group 2 ILCs present in healthy human skin that are enriched in lesional human skin from atopic dermatitis (AD) patients. Group 2 ILCs were also found in normal murine skin and were critical for the development of inflammation in a murine model of AD-like disease. Remarkably, in contrast to group 2 ILC responses in the intestine and lung, which are critically regulated by IL-33 and IL-25, group 2 ILC responses in the skin and skin-draining lymph nodes were independent of these canonical cytokines but were critically dependent on thymic stromal lymphopoietin (TSLP). Collectively, these results demonstrate an essential role for IL-33- and IL-25-independent group 2 ILCs in promoting skin inflammation.
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