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dc.contributor.author Futosi Krisztina
dc.contributor.author Fodor Szabina
dc.contributor.author Mócsai Attila
dc.date.accessioned 2016-09-20T08:06:35Z
dc.date.available 2016-09-20T08:06:35Z
dc.date.issued 2013
dc.identifier 84890114310
dc.identifier.citation pagination=1185-1197; journalVolume=17; journalIssueNumber=4; journalTitle=INTERNATIONAL IMMUNOPHARMACOLOGY;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/2631
dc.identifier.uri doi:10.1016/j.intimp.2013.11.010
dc.description.abstract Neutrophils play a critical role in the host defense against bacterial and fungal infections, but their inappropriate activation also contributes to tissue damage during autoimmune and inflammatory diseases. Neutrophils express a large number of cell surface receptors for the recognition of pathogen invasion and the inflammatory environment. Those include G-protein-coupled chemokine and chemoattractant receptors, Fc-receptors, adhesion receptors such as selectins/selectin ligands and integrins, various cytokine receptors, as well as innate immune receptors such as Toll-like receptors and C-type lectins. The various cell surface receptors trigger very diverse signal transduction pathways including activation of heterotrimeric and monomeric G-proteins, receptor-induced and store-operated Ca2 + signals, protein and lipid kinases, adapter proteins and cytoskeletal rearrangement. Here we provide an overview of the receptors involved in neutrophil activation and the intracellular signal transduction processes they trigger. This knowledge is crucial for understanding how neutrophils participate in antimicrobial host defense and inflammatory tissue damage and may also point to possible future targets of the pharmacological therapy of neutrophil-mediated autoimmune or inflammatory diseases. © 2013 The Authors.
dc.relation.ispartof urn:issn:1567-5769
dc.title Reprint of Neutrophil cell surface receptors and their intracellular signal transduction pathways
dc.type Journal Article
dc.date.updated 2015-11-24T10:47:50Z
dc.language.rfc3066 en
dc.identifier.mtmt 2500573
dc.identifier.wos 000329378800026
dc.contributor.department SE/AOK/I/Élettani Intézet
dc.contributor.institution Semmelweis Egyetem


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