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      ICOS:ICOS-ligand interaction is required for type 2 innate lymphoid cell function, homeostasis, and induction of airway hyperreactivity.

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          Abstract

          Allergic asthma is caused by Th2-cell-type cytokines in response to allergen exposure. Type 2 innate lymphoid cells (ILC2s) are a newly identified subset of immune cells that, along with Th2 cells, contribute to the pathogenesis of asthma by producing copious amounts of IL-5 and IL-13, which cause eosinophilia and airway hyperreactivity (AHR), a cardinal feature of asthma. ILC2s express ICOS, a T cell costimulatory molecule with a currently unknown function. Here we showed that a lack of ICOS on murine ILC2s and blocking the ICOS:ICOS-ligand interaction in human ILC2s reduced AHR and lung inflammation. ILC2s expressed both ICOS and ICOS-ligand, and the ICOS:ICOS-ligand interaction promoted cytokine production and survival in ILC2s through STAT5 signaling. Thus, ICOS:ICOS-ligand signaling pathway is critically involved in ILC2 function and homeostasis.

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          Author and article information

          Journal
          Immunity
          Immunity
          1097-4180
          1074-7613
          Mar 17 2015
          : 42
          : 3
          Affiliations
          [1 ] Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, Los Angeles, California 90033, USA.
          [2 ] Janssen Research and Development, San Diego, California 92121, USA.
          [3 ] Department of Medical Oncology, Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA.
          [4 ] Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA.
          [5 ] Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, Los Angeles, California 90033, USA. Electronic address: akbari@usc.edu.
          Article
          S1074-7613(15)00082-5 NIHMS667453
          10.1016/j.immuni.2015.02.007
          25769613
          ddd29cc7-942e-4e56-b8e9-658bca94ae75
          Copyright © 2015 Elsevier Inc. All rights reserved.

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