T reg cell-intrinsic requirements for ST2 signaling in health and neuroinflammation.

T reg cell-intrinsic requirements for ST2 signaling in health and neuroinflammation.
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t对健康和神经炎症中的ST2信号传导的核对细胞中心需求。

DOI:
10.1084/jem.20201234
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发表时间:
2021-02-01
期刊:
The Journal of experimental medicine
影响因子:
--
通讯作者:
Rudensky AY
Rudensky AY
中科院分区:
其他
文献类型:
--
作者:
Hemmers S;Schizas M;Rudensky AY

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ST2 expression was largely dispensable for T reg cell accumulation and maintenance in tissues at steady state. However, ST2 deficiency limited to T reg cells was important in limiting the size of IL-17A–producing γδT cells in a mouse model of neuroinflammation. ST2, the receptor for the alarmin IL-33, is expressed by a subset of regulatory T (T reg) cells residing in nonlymphoid tissues, and these cells can potently expand upon provision of exogenous IL-33. Whether the accumulation and residence of T reg cells in tissues requires their cell-intrinsic expression of and signaling by ST2, or whether indirect IL-33 signaling acting on other cells suffices, has been a matter of contention. Here, we report that ST2 expression on T reg cells is largely dispensable for their accumulation and residence in nonlymphoid organs, including the visceral adipose tissue (VAT), even though cell-intrinsic sensing of IL-33 promotes type 2 cytokine production by VAT-residing T reg cells. In addition, we uncovered a novel ST2-dependent role for T reg cells in limiting the size of IL-17A–producing γδT cells in the CNS in a mouse model of neuroinflammation, experimental autoimmune encephalomyelitis (EAE). Finally, ST2 deficiency limited to T reg cells led to disease exacerbation in EAE.
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