S1P-dependent interorgan trafficking of group 2 innate lymphoid cells supports host defense

Innate lymphoid cells (ILCs) are innate counterparts of adaptive T lymphocytes, contributing to host defense, tissue repair, metabolic homeostasis, and inflammatory diseases. ILCs have been considered to be tissue-resident cells, but whether ILCs move between tissue sites during infection has been u...

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Published in:Science (American Association for the Advancement of Science) Vol. 359; no. 6371; p. 114
Main Authors: Huang, Yuefeng, Mao, Kairui, Chen, Xi, Sun, Ming-An, Kawabe, Takeshi, Li, Weizhe, Usher, Nicholas, Zhu, Jinfang, Urban, Jr, Joseph F, Paul, William E, Germain, Ronald N
Format: Journal Article
Language:English
Published: United States 05.01.2018
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ISSN:1095-9203, 1095-9203
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Summary:Innate lymphoid cells (ILCs) are innate counterparts of adaptive T lymphocytes, contributing to host defense, tissue repair, metabolic homeostasis, and inflammatory diseases. ILCs have been considered to be tissue-resident cells, but whether ILCs move between tissue sites during infection has been unclear. We show here that interleukin-25- or helminth-induced inflammatory ILC2s are circulating cells that arise from resting ILC2s residing in intestinal lamina propria. They migrate to diverse tissues based on sphingosine 1-phosphate (S1P)-mediated chemotaxis that promotes lymphatic entry, blood circulation, and accumulation in peripheral sites, including the lung, where they contribute to anti-helminth defense and tissue repair. This ILC2 expansion and migration is a behavioral parallel to the antigen-driven proliferation and migration of adaptive lymphocytes to effector sites and indicates that ILCs complement adaptive immunity by providing both local and distant tissue protection during infection.
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ISSN:1095-9203
1095-9203
DOI:10.1126/science.aam5809