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Crucial discovery in regulating dysregulated & overamplified inflammation


Under the leadership of WANG Jing, Researcher, and ARASE Hisashi, Professor, Research Institute for Microbial Diseases, Immunology Frontier Research Center, Osaka University, a group of researchers has discovered that PILRα regulated neurtophil infiltration during inflammation via modulation of integrin activation -- a first-in-the-world research result, a finding crucial to controlling and/or preventing dysregulated or overamplified inflammatory response.


"Acute inflammatory responses are important in host defense, whereas dysregulated inflammation results in life-threatening complications. Here we found that paired immunoglobulin-like type 2 receptor alpha (PILRα), an inhibitory receptor containing immunoreceptor tyrosine-based inhibitory motifs (ITIMs), negatively regulated neutrophil infiltration during inflammation. Pilra−/− mice had increased neutrophil recruitment to inflammatory sites and were highly susceptible to endotoxin shock. Pilra−/− neutrophils showed enhanced transmigration ability and increased adhesion to the β2 integrin ligand ICAM-1. PILRα expressed on neutrophils constitutively associated in cis with its ligands, resulting in clustering of PILRα during stimulation with a chemoattractant. Clustering of PILRα enhanced ITIM-mediated signaling, thus modulating β2 integrin inside-out activation. These data demonstrate that neutrophil recruitment in inflammatory responses is regulated by PILRα via modulation of integrin activation."


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To learn more about this research, please read the full research report entitled "Neutrophil infiltration during inflammation is regulated by PILRα via modulation of integrin activation" at this page of the Nature Immunology website.

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