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T and B cell responses to self antigens (including antigens in joint tissues)

Lymphocytes, antibodies and ] immune complexes enter joint

Molecular Immunology

FIGURE 18-10 A model for the pathogenesis of rheumatoid arthritis. According to this hypothesis, citrullinated proteins induced by environmental stimuli elicit T cell and antibody responses in genetically susceptible individuals. The T cells and antibodies enter joints, respond to the self proteins, and cause tissue injury mainly by cytokine secretion and perhaps also by antibody-dependent effector mechanisms. Protein modifications other than citrullination may lead to the same result.

Destruction of cartilage and bone

FIGURE 18-10 A model for the pathogenesis of rheumatoid arthritis. According to this hypothesis, citrullinated proteins induced by environmental stimuli elicit T cell and antibody responses in genetically susceptible individuals. The T cells and antibodies enter joints, respond to the self proteins, and cause tissue injury mainly by cytokine secretion and perhaps also by antibody-dependent effector mechanisms. Protein modifications other than citrullination may lead to the same result.

self proteins are also present in joints, the T cells and antibodies attack the joints. TH17 and perhaps TH1 cells secrete cytokines that recruit leukocytes into the joint and activate synovial cells to produce collagenases and other enzymes. The net result is the progressive destruction of cartilage and bone. The immune response in the joint may be strong enough that tertiary lymphoid tissues form in the synovium, and these may maintain and propagate the local inflammatory reaction.

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Arthritis Joint Pain

Arthritis Joint Pain

Arthritis is a general term which is commonly associated with a number of painful conditions affecting the joints and bones. The term arthritis literally translates to joint inflammation.

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