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dc.contributor.author Németh, Tamás
dc.contributor.author Futosi, Krisztina
dc.contributor.author Szilveszter, Kata
dc.contributor.author Vilinovszki O
dc.contributor.author Kiss-Pápai L
dc.contributor.author Mócsai, Attila
dc.date.accessioned 2018-06-21T09:36:31Z
dc.date.available 2018-06-21T09:36:31Z
dc.date.issued 2018
dc.identifier 85044155119
dc.identifier.citation pagination=555, pages: 10; journalVolume=9; journalIssueNumber=MAR; journalTitle=FRONTIERS IN IMMUNOLOGY;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/5462
dc.identifier.uri doi:10.3389/fimmu.2018.00555
dc.description.abstract Autoantibody production and autoantibody-mediated inflammation are hallmarks of a number of autoimmune diseases. The K/BxN serum-transfer arthritis is one of the most widely used models of the effector phase of autoantibody-induced pathology. Several hematopoietic lineages including neutrophils, platelets, and mast cells have been proposed to contribute to inflammation and tissue damage in this model. We have previously shown that the Syk tyrosine kinase is critically involved in the development in K/BxN serum-transfer arthritis and bone marrow chimeric experiments indicated that Syk is likely involved in one or more hematopoietic lineages during the disease course. The aim of the present study was to further define the lineage(s) in which Syk expression is required for autoantibody-induced arthritis. To this end, K/BxN serum-transfer arthritis was tested in conditional mutant mice in which Syk was deleted in a lineage-specific manner from neutrophils, platelets, or mast cells. Combination of the MRP8-Cre, PF4-Cre, or Mcpt5-Cre transgene with floxed Syk alleles allowed efficient and selective deletion of Syk from neutrophils, platelets, or mast cells, respectively. This has also been confirmed by defective Syk-dependent in vitro functional responses of the respective cell types. In vivo studies revealed nearly complete defect of the development of K/BxN serum-transfer arthritis upon neutrophil-specific deletion of Syk. By contrast, Syk deletion from platelets or mast cells did not affect the development of K/BxN serum-transfer arthritis. Our results indicate that autoantibody-induced arthritis requires Syk expression in neutrophils, whereas, contrary to prior assumptions, Syk expression in platelets or mast cells is dispensable for disease development in this model. © 2018 Németh, Futosi, Szilveszter, Vilinovszki, Kiss-Pápai and Mócsai.
dc.relation.ispartof urn:issn:1664-3224
dc.title Lineage-specific analysis of Syk function in autoantibody-induced arthritis
dc.type Journal Article
dc.date.updated 2018-05-18T13:03:43Z
dc.language.rfc3066 en
dc.identifier.mtmt 3374084
dc.contributor.department SE/AOK/I/ÉI/MTA-SE Lendület Gyulladásélettani Kutatócsoport
dc.contributor.department SE/AOK/I/Élettani Intézet
dc.contributor.institution Semmelweis Egyetem
dc.mtmt.swordnote FELTÖLTŐ: Sonnevend Kinga - sonnevend.kinga@med.semmelweis-univ.hu


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