EphA2 Phosphorylates NLRP3 and Inhibits Inflammasomes in Airway Epithelial Cells

ABSTRACT: Inflammasomes are intracellular complexes that form in the cytosol of inflammatory cells. NLRP3 is one of the sensor proteins in the complex that can recognize a wide variety of stimuli ranging from microbial components to environmental particulates. Here, we report that in mouse airway epithelial cells (AECs), inflammasome activation is inhibited by EphA2, a member of the transmembrane tyrosine kinase receptor family via tyrosine phosphorylation of NLRP3 in a model of reovirus infection. We find that EphA2 depletion markedly enhances Interleukin-1? (IL-1?) and interleukin-18 (IL-18) production in response to the virus. EphA2-/- mice show stronger inflammatory infiltration and enhanced inflammasome activation upon viral infection, and aggravated asthma symptoms upon ovalbumin (ova) inducti

SUBMITTER: Prof. Mu-Sheng Zeng 

PROVIDER: S-SCDT-EMBOR-2019-49666V1 | biostudies-other |

REPOSITORIES: biostudies-other