Unknown

Dataset Information

0

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

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.

SUBMITTER: Maazi H 

PROVIDER: S-EPMC4366271 | biostudies-literature | 2015 Mar

REPOSITORIES: biostudies-literature

Json Xml
altmetric image

Publications

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

Maazi Hadi H   Patel Nisheel N   Sankaranarayanan Ishwarya I   Suzuki Yuzo Y   Rigas Diamanda D   Soroosh Pejman P   Freeman Gordon J GJ   Sharpe Arlene H AH   Akbari Omid O  

Immunity 20150310 3

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  ...[more]

Similar Datasets

Unknown Innate Lymphoid Cells Are Required to Induce Airway Hyperreactivity in a Murine Neutrophilic Asthma Model.
| S-EPMC8965562 | biostudies-literature
Unknown Type 2 innate lymphoid cell suppression by regulatory T cells attenuates airway hyperreactivity and requires inducible T-cell costimulator-inducible T-cell costimulator ligand interaction.
| S-EPMC5378695 | biostudies-literature
Unknown Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity.
| S-EPMC3246069 | biostudies-literature
Unknown Cannabinoid receptor 2 engagement promotes group 2 innate lymphoid cell expansion and enhances airway hyperreactivity.
| S-EPMC9013728 | biostudies-literature
Unknown Interleukin-17-producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity.
| S-EPMC3912313 | biostudies-literature
Unknown Programmed cell death ligand 2 regulates TH9 differentiation and induction of chronic airway hyperreactivity.
| S-EPMC3651917 | biostudies-literature
Unknown Mesenchymal stem cells regulate type 2 innate lymphoid cells via regulatory T cells through ICOS-ICOSL interaction.
| S-EPMC8360040 | biostudies-literature
Unknown The polymeric mucin Muc5ac is required for allergic airway hyperreactivity.
| S-EPMC4333679 | biostudies-literature
Unknown TNFR2 Signaling Enhances ILC2 Survival, Function, and Induction of Airway Hyperreactivity.
| S-EPMC6940205 | biostudies-literature
Unknown Type 2 innate lymphoid cells control eosinophil homeostasis.
| S-EPMC3795960 | biostudies-other