2003, Number 2
Etiopathogenic hypothesis of the rheumatoid arthritis
Berrón PRD, Yamazaki NMA, Covarrubias CRM, Cortés GRM
Full text
Language: Spanish
References: 8
Page: 5-7
PDF size: 260.88 Kb.
ABSTRACT
Rheumatoid arthritis is the most frequent systemic autoimmune disease, with an enormous administrative and medical importance. Despite tons of information involving genetical and environmental factors participating in its ethiopathogenesis, there isn’t any satisfactory explanation. Based on information of the last six years we propose a hypothesis that involves a genetical defect of clonal deletion in the embryo, allowing the recognition of HLA class II molecules by own T-cells. Supporting this fact there are studies with transgenic mice and T-cell defects in patients with RA, the defect is amplified by environmental stimuli, mainly infectious stimuli, that shares epytopes with HLA molecules, they are captured in the joints, acting like low temperature filters, and that’s why we observe that the joints affected are distal, symmetrical, with high mobility and augments blood flow. With synoviocytes type A presenting HLA type II molecules on its surface, inflammation takes place with cellular recruitment, stimuli for degraded structures in the joint, neurohormones and production in situ of autoantibodies by B-cells and when these autoantibodies are in the circulation, extra-articular manifestations take place. This hypothesis can explain many phenomena of the disease and it is capable to be confirmed experimentally.REFERENCES
Debaz H, Olivo A, Vázquez-García MN, de la Rosa G, Hernandez A, Lino L, Burgos R, Fernández-Vina M, Stastny P, Gorodezky C. Relevant residues of Drbeta1 third hypervariable region contributing to the expression and to severity of reumathoid arthritis (RA) in Mexicans. Human Immunol 1998; 59(5): 287-294.