期刊
IMMUNITY
卷 43, 期 1, 页码 161-174出版社
CELL PRESS
DOI: 10.1016/j.immuni.2015.05.019
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资金
- NIH [AI026918, AI030663, AI078869, HL107202, K08DK101604]
- UCSF Diabetes Family Fund
- UCSF REAC Pilot Grant
- Sandler Asthma Basic Research Center at UCSF
- Howard Hughes Medical Institute
Group 2 innate lymphoid cells (ILC2s) and regulatory T (Treg) cells are systemically induced by helminth infection but also sustain metabolic homeostasis in adipose tissue and contribute to tissue repair during injury. Here we show that interleukin-33 (IL-33) mediates activation of ILC2s and Treg cells in resting adipose tissue, but also after helminth infection or treatment with IL-2. Unexpectedly, ILC2-intrinsic IL-33 activation was required for Treg cell accumulation in vivo and was independent of ILC2 type 2 cytokines but partially dependent on direct co-stimulatory interactions via ICOSL-ICOS. IFN-gamma inhibited ILC2 activation and Treg cell accumulation by IL-33 in infected tissue, as well as adipose tissue, where repression increased with aging and high-fat diet-induced obesity. IL-33 and ILC2s are central mediators of type 2 immune responses that promote tissue and metabolic homeostasis, and IFN-gamma suppresses this pathway, likely to promote inflammatory responses and divert metabolic resources necessary to protect the host.
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