rium-primed mononuclear cells in the joints of our patient: The joint is the place where cross-reactive antigenic material is amply available in the form of cartilage or, in later stages, degradation products thereof. Bacterium-(and thus, cartilage)-reactive T cells circulate through the body, enter the joint, and may be trapped there in an antigen-specific manner.
These data tempt us t o suggest the following mechanism as a possible explanation of certain forms of chronic arthritis. An individual who experiences a bacterial infection (which might go unnoticed) will mount an immune response against the infecting agent. Due to the similar structure of bacterial cell walls and cartilage proteoglycans, this defensive immune response might display some harmful autoimmune characteristics through a reactivity against cartilage components. This cross-reactive autoimmune response will come to full expression in an individual who has some aberrant condition, such as certain major histocompatibility complex haplotypes, joint trauma, a defective suppressor/ feedback circuit, or a combination thereof.
An arthritis induced by bacteria can be reactivated by each subsequent triggering by another (unrelated) bacterium or by cartilage components released after joint damage, and thus can become chronic. We believe that T cells play an important role in this autoimmune response, and therefore, the same cells might be of major importance in the chronicity of arthritis .