期刊
IMMUNITY
卷 48, 期 6, 页码 1195-+出版社
CELL PRESS
DOI: 10.1016/j.immuni.2018.05.003
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资金
- UK Medical Research Council [U105178805]
- Wellcome Trust [100963/Z/13/Z, 17966/Z/2008, 204622/Z/16/Z]
- EMBL
- ERC
- Cancer Research UK
- MRC [MC_U105178805] Funding Source: UKRI
- Wellcome Trust [204622/Z/16/Z] Funding Source: Wellcome Trust
The local regulation of type 2 immunity relies on dialog between the epithelium and the innate and adaptive immune cells. Here we found that alarm-ininduced expression of the co-stimulatory molecule OX40L on group 2 innate lymphoid cells (ILC2s) provided tissue-restricted T cell co-stimulation that was indispensable for Th2 and regulatory T (Treg) cell responses in the lung and adipose tissue. Interleukin (IL)-33 administration resulted in organ-specific surface expression of OX40L on ILC2s and the concomitant expansion of Th2 and Treg cells, which was abolished upon deletion of OX40L on ILC2s (Il7ra(Cre/+)Tnfsf4(fl/fl) mice). Moreover, Il7ra(Cre/+) Tnfsf4(fl/fl) mice failed to mount effective Th2 and Treg cell responses and corresponding adaptive type 2 pulmonary inflammation arising from Nippostrongylus brasiliensis infection or allergen exposure. Thus, the increased expression of OX40L in response to IL-33 acts as a licensing signal in the orchestration of tissue-specific adaptive type 2 immunity, without which this response fails to establish.
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