Etiology of rheumatoid arthritis.
The major thesis of the proposed hypothesis is that in the absence of microbial material synovial macrophages in rheumatoid arthritis patients continue to release interleukin 1, which perpetuates the inflammation so characteristic of the disease. Its release is suggested to result from an altered synovial macrophage glutathione metabolism brought about by the action of interleukin 1 on host copper metabolism. Three anti-rheumatic drugs are suggested to act at different points in this pathogenic chain reaction. Alclofenac on interleukin 1, gold thiolates on copper-inhibited macrophage glutathione reductase, and D-penicillamine on IgC catabolism. Drawing upon the hypothesis some suggestions are made for drug design.
D001172:Arthritis, Rheumatoid / Q000209:etiology*; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis; D008262:Macrophage Activation; D008264:Macrophages / Q000502:physiology; D013582:Synovial Fluid / Q000166:cytology
D007375:Interleukin-1