A tissue checkpoint regulates type 2 immunity

作者：Van Dyken Steven J; Nus**aum Jesse C; Lee Jinwoo; Molofsky Ari B; Liang Hong Erh; Pollack Joshua L; Gate Rachel E; Haliburton Genevieve E; Ye Chun J; Marson Alexander; Erle David J; Locksley Richard M

来源：Nature Immunology, 2016, 17(12): 1381-1387.

DOI：10.1038/ni.3582

Group 2 innate lymphoid cells (ILC2s) and CD4(+) type 2 helper T cells (T(H)2 cells) are defined by their similar effector cytokines, which together mediate the features of allergic immunity. We found that tissue ILC2s and T(H)2 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 T(H)2 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.

• 出版日期2016-12