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dc.contributor.authorGul, A
dc.date.accessioned2021-03-04T17:22:41Z
dc.date.available2021-03-04T17:22:41Z
dc.date.issued2001
dc.identifier.citationGul A., "Behcet's disease: An update on the pathogenesis", CLINICAL AND EXPERIMENTAL RHEUMATOLOGY, cilt.19, sa.5, 2001
dc.identifier.issn0392-856X
dc.identifier.othervv_1032021
dc.identifier.otherav_85d47d88-c42c-465f-8f33-38047443b3a0
dc.identifier.urihttp://hdl.handle.net/20.500.12627/90978
dc.description.abstractBehcet's disease is a chronic inflammatory disorder of unknown etiology. It has long been postulated that immunological abnormalities, which are possibly induced by, microbial pathogens in genetically susceptible individuals, are important in its pathogenesis. Recent findings have both supported the significance of genetic factors and better defined the nature of inflammation in Behcet's disease. Molecular genetic studies have strengthened the primary association of HLA-B51 with Behcet's disease. The exact pathogenic mechanism of the HLA-B51 molecule is still unknown, and its contribution to the overall genetic susceptibility to Behcet's disease is estimated to be less than 20%. Spontaneous and/or induced overexpression of pro-inflammatory cytokines (mainly Th1 type)from various cellular sources seems responsible for the enhanced inflammatory reaction in Behcet's disease, and it may be associated with the genetic susceptibility . An antigen-driven immune response superimposed on this primed-state and induced by heat shock proteins or other peptides,from different strains of streptoccocci or other microbial agents has been suggested to trigger manifestations of Behcet's disease. Endothelial activation/injury and the resultant occlusive vasculopathy may also contribute to the tissue damage.
dc.language.isoeng
dc.subjectİmmünoloji ve Romatoloji
dc.subjectKlinik Tıp (MED)
dc.subjectTıp
dc.subjectSağlık Bilimleri
dc.subjectDahili Tıp Bilimleri
dc.subjectİç Hastalıkları
dc.subjectROMATOLOJİ
dc.subjectKlinik Tıp
dc.titleBehcet's disease: An update on the pathogenesis
dc.typeMakale
dc.relation.journalCLINICAL AND EXPERIMENTAL RHEUMATOLOGY
dc.contributor.department, ,
dc.identifier.volume19
dc.identifier.issue5
dc.contributor.firstauthorID162811


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