Rheumatoid arthritis (RA) results from dysregulation of the humoral and cell-mediated components of the immune system. Most patients produce antibodies called rheumatoid factors; these seropositive patients tend to have a more aggressive course than patients who are seronegative.
Immunoglobulins can activate the complemet system, which amplifies the immune response by enhancing chemotaxis, phagocytosis, and release of lymphokines by mononuclear cells that are then presented to T lymphocytes. The processed antigen is recognized by the major histocompatibility comples (MHC) proteins on the lymphocyte surface, resulting in activation of T and B cells.
Tumor necrosis factor (TNF), interleukin-1 (IL-1), and interleukin-6 (IL-6) are proinflammatory cytokines important in the initiation and continuance of inflammation.
Activated T cells produce cytotoxins, which are directly toxic to tissues, and cytokines, which stimulate further activation of inflammatory processes and attract cells to areas of inflammation. Macrophages are stimulated to release prostaglandins and cytotoxins.
Activated B cells produce plasma cells, which form antibodies that, in combination with complement, result in accumulation of polymorphonuclear leukocytes (PMNs). PMNs release cytotoxins, oxygen free radicals, and hydroxyl radicals that promote cellular damage to synovium and bone.
Vasoactive substances (histamine, kinins, and prostaglandins) are released at sites of inflammation, increasing blood flow and vascular permeability. This causes edema, warmth, erythema, and pain and makes it easier for granulocytes to pass from blood vessels to sites of inflammation.
Chronic inflammation of the synovial tissue lining the joint capsule results in tissue proliferation (pannus formation). Pannus invades cartilage and eventually the bone surface, producing erosions of bone and cartilage and leading to joint destruction. The end results may be loss of joint space, loss of joint motion, bony fusion (ankylosis), joint subluxation, tendon contractures, and chronic deformity.
Immunoglobulins can activate the complemet system, which amplifies the immune response by enhancing chemotaxis, phagocytosis, and release of lymphokines by mononuclear cells that are then presented to T lymphocytes. The processed antigen is recognized by the major histocompatibility comples (MHC) proteins on the lymphocyte surface, resulting in activation of T and B cells.
Tumor necrosis factor (TNF), interleukin-1 (IL-1), and interleukin-6 (IL-6) are proinflammatory cytokines important in the initiation and continuance of inflammation.
Activated T cells produce cytotoxins, which are directly toxic to tissues, and cytokines, which stimulate further activation of inflammatory processes and attract cells to areas of inflammation. Macrophages are stimulated to release prostaglandins and cytotoxins.
Activated B cells produce plasma cells, which form antibodies that, in combination with complement, result in accumulation of polymorphonuclear leukocytes (PMNs). PMNs release cytotoxins, oxygen free radicals, and hydroxyl radicals that promote cellular damage to synovium and bone.
Vasoactive substances (histamine, kinins, and prostaglandins) are released at sites of inflammation, increasing blood flow and vascular permeability. This causes edema, warmth, erythema, and pain and makes it easier for granulocytes to pass from blood vessels to sites of inflammation.
Chronic inflammation of the synovial tissue lining the joint capsule results in tissue proliferation (pannus formation). Pannus invades cartilage and eventually the bone surface, producing erosions of bone and cartilage and leading to joint destruction. The end results may be loss of joint space, loss of joint motion, bony fusion (ankylosis), joint subluxation, tendon contractures, and chronic deformity.
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