@article {542001,
	title = {ICOS:ICOS-ligand interaction is required for type 2 innate lymphoid cell function, homeostasis, and induction of airway hyperreactivity.},
	journal = {Immunity},
	volume = {42},
	number = {3},
	year = {2015},
	month = {2015 Mar 17},
	pages = {538-51},
	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.},
	keywords = {Animals, Asthma, Female, Gene Expression Regulation, Homeostasis, Humans, Immunity, Innate, Inducible T-Cell Co-Stimulator Ligand, Inducible T-Cell Co-Stimulator Protein, Interleukin-13, Interleukin-2, Interleukin-5, Interleukins, Lymphocytes, Mice, Transgenic, Respiratory System, Signal Transduction, STAT5 Transcription Factor},
	issn = {1097-4180},
	doi = {10.1016/j.immuni.2015.02.007},
	author = {Maazi, Hadi and Patel, Nisheel and Sankaranarayanan, Ishwarya and Suzuki, Yuzo and Rigas, Diamanda and Soroosh, Pejman and Freeman, Gordon J and Sharpe, Arlene H and Akbari, Omid}
}
