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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Vydáno v:	Science (American Association for the Advancement of Science) Ročník 359; číslo 6371; s. 114
Hlavní autoři:	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
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States 05.01.2018
Témata:	Adaptive Immunity Animals Cell Proliferation Chemotaxis - immunology Female Fingolimod Hydrochloride - pharmacology Homeodomain Proteins - genetics Homeostasis Immunity, Innate Immunosuppressive Agents - pharmacology Interleukin-17 - immunology Intestines - immunology Lung - immunology Lymphocytes - immunology Lysophospholipids - immunology Mice Mice, Inbred C57BL Mice, Mutant Strains Mucous Membrane - immunology Nippostrongylus - immunology Sphingosine - analogs & derivatives Sphingosine - immunology Strongylida Infections - immunology T-Lymphocytes - immunology
ISSN:	1095-9203, 1095-9203
On-line přístup:	Zjistit podrobnosti o přístupu
Tagy:	Přidat tag Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!

Abstract	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.
AbstractList	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. 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.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.
Author	Chen, Xi Urban, Jr, Joseph F Usher, Nicholas Germain, Ronald N Zhu, Jinfang Paul, William E Mao, Kairui Sun, Ming-An Kawabe, Takeshi Huang, Yuefeng Li, Weizhe
Author_xml	– sequence: 1 givenname: Yuefeng orcidid: 0000-0002-3860-5430 surname: Huang fullname: Huang, Yuefeng organization: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health, Bethesda, MD 20892, USA – sequence: 2 givenname: Kairui surname: Mao fullname: Mao, Kairui organization: Laboratory of Systems Biology, NIAID, National Institutes of Health, Bethesda, MD 20892, USA – sequence: 3 givenname: Xi surname: Chen fullname: Chen, Xi organization: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health, Bethesda, MD 20892, USA – sequence: 4 givenname: Ming-An orcidid: 0000-0002-4661-3027 surname: Sun fullname: Sun, Ming-An organization: Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA – sequence: 5 givenname: Takeshi orcidid: 0000-0001-7173-4472 surname: Kawabe fullname: Kawabe, Takeshi organization: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health, Bethesda, MD 20892, USA – sequence: 6 givenname: Weizhe surname: Li fullname: Li, Weizhe organization: Laboratory of Systems Biology, NIAID, National Institutes of Health, Bethesda, MD 20892, USA – sequence: 7 givenname: Nicholas orcidid: 0000-0001-8779-519X surname: Usher fullname: Usher, Nicholas organization: Department of Undergraduate Biology, Cornell University, Ithaca, NY 14853, USA – sequence: 8 givenname: Jinfang surname: Zhu fullname: Zhu, Jinfang organization: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health, Bethesda, MD 20892, USA – sequence: 9 givenname: Joseph F orcidid: 0000-0002-1590-8869 surname: Urban, Jr fullname: Urban, Jr, Joseph F organization: Diet, Genomics, and Immunology Laboratory, Beltsville Human Nutrition Research Center, Agricultural Research Service, U.S. Department of Agriculture (USDA), Beltsville, MD 20705, USA – sequence: 10 givenname: William E surname: Paul fullname: Paul, William E organization: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health, Bethesda, MD 20892, USA – sequence: 11 givenname: Ronald N orcidid: 0000-0003-1495-9143 surname: Germain fullname: Germain, Ronald N email: yuefeng.huang@nih.gov, rgermain@niaid.nih.gov organization: Laboratory of Systems Biology, NIAID, National Institutes of Health, Bethesda, MD 20892, USA
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/29302015$$D View this record in MEDLINE/PubMed
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References	29466752 - Immunity. 2018 Feb 20;48(2):200-201 29302003 - Science. 2018 Jan 5;359(6371):36-37
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SubjectTerms	Adaptive Immunity Animals Cell Proliferation Chemotaxis - immunology Female Fingolimod Hydrochloride - pharmacology Homeodomain Proteins - genetics Homeostasis Immunity, Innate Immunosuppressive Agents - pharmacology Interleukin-17 - immunology Intestines - immunology Lung - immunology Lymphocytes - immunology Lysophospholipids - immunology Mice Mice, Inbred C57BL Mice, Mutant Strains Mucous Membrane - immunology Nippostrongylus - immunology Sphingosine - analogs & derivatives Sphingosine - immunology Strongylida Infections - immunology T-Lymphocytes - immunology
Title	S1P-dependent interorgan trafficking of group 2 innate lymphoid cells supports host defense
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