title: Immunopathogenesis of Behçet's disease.
abstract: A working hypothesis is postulated for the immunopathogenesis of Behçet's disease (BD). Microbial infection induced stress upregulates HSP65 and MICA gene product which stimulate gamma delta and alpha beta T cell receptor positive cells, to generate effector and suppressor T cells (fig. 1). These activated T cells, antibodies and neutrophils induce cytokines to modulate the immune response. The end result of these complex cellular and cytokine immune interactions in HLA-B51 or genetically related subjects is to induce pathological changes consistent with BD.
authors.affiliation: Department of Immunobiology, Guy's Hospital Medical School, Guy's Hospital, London. thomas.lehner@kcl.ac.uk
authors.forename: T
authors.initials: T
authors.lastname: Lehner
mesh_terms: D001528:Behcet Syndrome / Q000235:genetics / Q000276:immunology*; D016207:Cytokines / Q000096:biosynthesis; D006360:Heat-Shock Proteins / Q000096:biosynthesis; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis
chemical_list: D016207:Cytokines; D006360:Heat-Shock Proteins; D018799:Intercellular Adhesion Molecule-1