Exaggerated inflammatory responsiveness plays a part in the pathogenesis of HLA-B27 linked diseases--hypothesis.
Ankylosing spondylitis, acute anterior uveitis and reactive arthritides, including enteroarthritis and uroarthritis , are all associated with the human leucocyte antigen (HLA) B27. The pathogenesis of these diseases is not known, but it may involve inflammatory responsiveness of the host. In an acute inflammatory reaction, neutrophils are considered to cause tissue injury by both liberating lysosomal enzymes and generating toxic oxygen-derived free radicals. Furthermore, they may regulate both capillary permeability and the rate of vasodilatation at the site of inflammation. Evidence has accumulated that neutrophil responses to a phlogistic stimulus are enhanced in HLA-27 positive subjects. We suggest that hyperreactive neutrophils trigger a vicious circle of inflammation and render the subjects susceptible to exaggerated tissue injury.
D001168:Arthritis / Q000276:immunology; D002199:Capillary Permeability; D002634:Chemotaxis, Leukocyte; D006680:HLA Antigens / Q000032:analysis*; D015796:HLA-B27 Antigen; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology; D013167:Spondylitis, Ankylosing / Q000276:immunology; D014605:Uveitis / Q000276:immunology; D014664:Vasodilation
D006680:HLA Antigens; D015796:HLA-B27 Antigen