Egyszerű nézet

dc.contributor.author Németh, Tamás
dc.contributor.author Mócsai, Attila
dc.contributor.author Lowell, Clifford
dc.date.accessioned 2016-08-23T06:17:20Z
dc.date.available 2016-08-23T06:17:20Z
dc.date.issued 2016
dc.identifier.citation pagination=174-186; journalVolume=28; journalIssueNumber=2; journalTitle=SEMINARS IN IMMUNOLOGY;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/3638
dc.identifier.uri doi:10.1016/j.smim.2016.04.001
dc.description.abstract Neutrophils have traditionally been thought to play only a peripheral role in the genesis of many autoimmune and inflammatory diseases. However, recent studies in a variety of animal models suggest that these cells are central to the initiation and propagation of autoimmunity. The use of mouse models, which allow either deletion of neutrophils or the targeting of specific neutrophil functions, has revealed the many complex ways these cells contribute to autoimmune/inflammatory processes. This includes generation of self antigens through the process of NETosis, regulation of T-cell and dendritic cell activation, production of cytokines such as BAFF that stimulate self-reactive B-cells, as well as indirect effects on epithelial cell stability. In comparing the many different autoimmune models in which neutrophils have been examined, a number of common underlying themes emerge - such as a role for neutrophils in stimulating vascular permeability in arthritis, encephalitis and colitis. The use of animal models has also stimulated the development of new therapeutics that target neutrophil functions, such as NETosis, that may prove beneficial in human disease. This review will summarize neutrophil contributions in a number of murine autoimmune/inflammatory disease models. © 2016 Elsevier Ltd.
dc.relation.ispartof urn:issn:1044-5323
dc.title Neutrophils in animal models of autoimmune disease
dc.type Journal Article
dc.date.updated 2016-08-18T09:53:48Z
dc.language.rfc3066 en
dc.identifier.mtmt 3057058
dc.identifier.wos 000376472500010
dc.identifier.scopus 84976448843
dc.identifier.pubmed 27067180
dc.contributor.department SE/AOK/I/Élettani Intézet
dc.contributor.department SE/AOK/I/ÉI/MTA-SE Lendület Gyulladásélettani Kutatócsoport
dc.contributor.institution Semmelweis Egyetem
dc.mtmt.swordnote FELTÖLTŐ: Sonnevend Kinga - sonnevend.kinga@med.semmelweis-univ.hu


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