ABSTRACT
The most challenging question for the study of rheumatoid arthritis concerns the specificity of the immune reactions that initiate and perpetuate the autoimmune pathology. These reactions are most likely dependent on both activated autoreactive T cells and certain autoreactive B cells. The anti-CII antibody response and development of arthritis have been extensively characterized in collagen-induced arthritis (CIA)-susceptible mouse and rat strains. One of the most interesting questions is whether there are any specific arthritogenic epitopes on the autologous CII molecule recognized by anti-CII antibodies. In rat and mouse species, only certain inbred strains are susceptible to the induction of CIA, suggesting a genetic linkage of CII responsiveness. Susceptibility for CIA is inherited polygenically, and there is evidence for at least four gene loci of importance: genes within Major Histocompatibility Complex, V genes coding for T cell receptors, complement genes, and possibly genes on sex chromosomes.
