Cutting edge: maresin-1 engages regulatory T cells to limit type 2 innate lymphoid cell activation and promote resolution of lung inflammation.
Cutting edge: maresin-1 engages regulatory T cells to limit type 2 innate lymphoid cell activation and promote resolution of lung inflammation.
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DOI：
10.4049/jimmunol.1402534
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发表时间：
2015-02-01
期刊：
影响因子：
--
通讯作者：
Levy BD
中科院分区：
文献类型：
--
作者：
Krishnamoorthy N;Burkett PR;Dalli J;Abdulnour RE;Colas R;Ramon S;Phipps RP;Petasis NA;Kuchroo VK;Serhan CN;Levy BD
哮喘是一种慢性炎症性疾病，无法解决。最近，2型先天性淋巴细胞（ILC 2）的关键作用与哮喘发病机制有关;然而，ILC 2的调节机制仍有待确定。在这里，代谢脂质组学的小鼠肺部确定内源性maresin 1（MaR 1）在自限性过敏性炎症的时间变化。外源性MaR 1减少了肺部炎症，ILC 2表达的白细胞介素-5和13，并增加双调蛋白。MaR 1增加调节性T细胞（Tcells）的从头产生，Tcells与ILC 2相互作用以TGF-β依赖性方式显著抑制细胞因子的产生。抗体介导的TcR的消耗中断了体内IL-13的ILC 2表达的MaR 1控制。总之，这些发现揭示了Tclad是ILC 2激活的有效调节剂; MaR 1靶向Tclad和ILC 2以抑制过敏性肺部炎症，这表明MaR 1是哮喘和其他慢性炎症性疾病的新的促缓解治疗方法的基础。
Asthma is a chronic inflammatory disease that fails to resolve. Recently, a key role for type 2 innate lymphoid cells (ILC2) was linked to asthma pathogenesis; however, mechanisms for ILC2 regulation remain to be determined. Here, metabololipidomics of murine lungs identified temporal changes in endogenous maresin 1 (MaR1) during self-limited allergic inflammation. Exogenous MaR1 reduced lung inflammation, ILC2 expression of interleukin-5 and 13, and increased amphiregulin. MaR1 augmented de novo generation of regulatory T cells (Tregs), which interacted with ILC2 to markedly suppress cytokine production in a TGF-β-dependent manner. Antibody-mediated depletion of Tregs interrupted MaR1 control of ILC2 expression of IL-13 in vivo. Together, the findings uncover Tregs as potent regulators of ILC2 activation; MaR1 targets Tregs and ILC2 to restrain allergic lung inflammation, suggesting MaR1 as the basis for a new pro-resolving therapeutic approach to asthma and other chronic inflammatory diseases.
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影响因子：
64.8
作者：
Bettelli, E;Carrier, YJ;Kuchroo, VK
通讯作者：
Kuchroo, VK
影响因子：
14.2
作者：
Barlow, Jillian L.;Bellosi, Agustin;McKenzie, Andrew N. J.
通讯作者：
McKenzie, Andrew N. J.
DOI：
10.1084/jem.20130071
发表时间：
2013-12-16
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Turner JE;Morrison PJ;Wilhelm C;Wilson M;Ahlfors H;Renauld JC;Panzer U;Helmby H;Stockinger B
通讯作者：
Stockinger B
影响因子：
32.4
作者：
Buckley, Christopher D.;Gilroy, Derek W.;Serhan, Charles N.
通讯作者：
Serhan, Charles N.
影响因子：
32.4
作者：
Sonnenberg GF;Artis D
通讯作者：
Artis D