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Immunity. 2015 Mar 17;42(3):538-51. doi: 10.1016/j.immuni.2015.02.007. Epub 2015 Mar 10.

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

Author information

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.

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.

PMID:
25769613
PMCID:
PMC4366271
DOI:
10.1016/j.immuni.2015.02.007
[Indexed for MEDLINE]
Free PMC Article

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