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10.1016/j.immuni.2015.02.007

http://scihub22266oqcxt.onion/10.1016/j.immuni.2015.02.007
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C4366271!4366271!25769613
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suck abstract from ncbi


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pmid25769613      Immunity 2015 ; 42 (3): 538-51
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  • ICOS:ICOS-Ligand interaction is required for type 2 innate lymphoid cell function, homeostasis and induction of airway hyperreactivity #MMPMID25769613
  • Maazi H; Patel N; Sankaranarayanan I; Suzuki Y; Rigas D; Soroosh P; Freeman GJ; Sharpe AH; Akbari O
  • Immunity 2015[Mar]; 42 (3): 538-51 PMID25769613show ga
  • 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 besides Th2 cells contribute to the pathogenesis of asthma by producing copious amount 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 currently unknown function. Here we showed that lack of ICOS on murine ILC2s and blocking 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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