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A tissue checkpoint regulates type 2 immunity.

Abstract：

:Group 2 innate lymphoid cells (ILC2s) and CD4+ type 2 helper T cells (TH2 cells) are defined by their similar effector cytokines, which together mediate the features of allergic immunity. We found that tissue ILC2s and TH2 cells differentiated independently but shared overlapping effector function programs that were mediated by exposure to the tissue-derived cytokines interleukin 25 (IL-25), IL-33 and thymic stromal lymphopoietin (TSLP). Loss of these three tissue signals did not affect lymph node priming, but abrogated the terminal differentiation of effector TH2 cells and adaptive lung inflammation in a T cell-intrinsic manner. Our findings suggest a mechanism by which diverse perturbations can activate type 2 immunity and reveal a shared local-tissue-elicited checkpoint that can be exploited to control both innate and adaptive allergic inflammation.

journal_name

Nat Immunol

journal_title

Nature immunology

authors

Van Dyken SJ,Nussbaum JC,Lee J,Molofsky AB,Liang HE,Pollack JL,Gate RE,Haliburton GE,Ye CJ,Marson A,Erle DJ,Locksley RM

doi

10.1038/ni.3582

subject

Has Abstract

pub_date

2016-12-01 00:00:00

pages

1381-1387

issue

12

eissn

1529-2908

issn

1529-2916

pii

ni.3582

journal_volume

17

pub_type

杂志文章

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