A tissue checkpoint regulates type 2 immunity

Steven J. Van Dyken, Jesse C. Nussbaum, Jinwoo Lee, Ari B. Molofsky, Hong Erh Liang, Joshua L. Pollack, Rachel E. Gate, Genevieve E. Haliburton, Chun J. Ye, Alexander Marson, David J. Erle, Richard M. Locksley

Research output: Contribution to journalArticlepeer-review

133 Scopus citations


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.

Original languageEnglish
Pages (from-to)1381-1387
Number of pages7
JournalNature immunology
Issue number12
StatePublished - Dec 1 2016


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