作者: Rodney A. Hughes , Andrew C. Keat
DOI: 10.1016/0049-0172(94)90075-2
关键词: Bacterial antigen 、 Lymphocyte proliferation 、 Immunology 、 Molecular mimicry 、 Reactive arthritis 、 Chlamydia trachomatis 、 Shigella flexneri 、 Antigen presentation 、 Medicine 、 Immune system 、 Anesthesiology and Pain Medicine 、 Rheumatology
摘要: This paper reviews advances in the understanding of pathogenesis reactive arthritis that have occurred over last decade. Inflammatory aseptic joint disease has been linked with prior infection initiated by many different species microorganisms. The presence intra-articular bacterial antigens now firmly established demonstration bacteria, fragments, DNA, RNA, and lipopolysaccharide joints patients arthritis. Chlamydia trachomatis, Salmonella enteritidis, Shigella flexneri all detected immunological techniques, although there is still some doubt as to form which they reach whether or not persist. A number phlogistic components could be acting arthritogens. Negative culture results from make it unlikely bacteria are viable, chlamydial DNA shown sexually acquired using polymerase chain reaction. use antimicrobial therapy treatment under review; data suggests long-term antibiotic warrants further study. role HLA-B27 discussed possible mechanisms interplay between germ gene. might confer susceptibility affecting immune other than classical antigen presentation. immunopathogenesis inflammation explored reference studies humoral cellular responses. Serological evidence support concept molecular mimicry far conclusive; relevant summarized. Lymphocyte proliferation experiments suggest presenting cells play an important role. Finally, our views on 1990s, areas new potentially fruitful future research presented.