Immunologic Manifestations of Rheumatoid Arthritis
المؤلف:
Mary Louise Turgeon
المصدر:
Immunology & Serology in Laboratory Medicine
الجزء والصفحة:
5th E, P426-428
2025-09-30
115
The current model of the pathogenesis of RA proposes that an infective agent or other stimulus binds to receptors on dendritic cells (DCs), which activates the innate immune system (Fig. 1). DCs migrate into lymph nodes and present anti gen to T lymphocytes, which are activated by two signals— the presentation of antigen and costimulation through CD28. Activated T lymphocytes proliferate and migrate into the joint. Subsequently, T lymphocytes produce interferon-γ (IFN-γ) and other proinflammatory cytokines. This in turn stimulates macrophages and other cells, including B lymphocytes. B cells appear to be pivotal in the pathogenesis of RA because they can be 10,000 times as potent as DCs in presenting antigen.
Fig1. Pathophysiologic role of cytokines and other mediators and their inhibitors in rheumatoid arthritis. MHC, Major histocompatibility complex; TNF, tumor necrosis factor. (Adapted from Scott DL, Kingsley GH: N Engl J Med 355:704–712, 2006.)
Stimulated macrophages and fibroblasts release cytokines, including tumor necrosis factor-α (TNF-α), a central component in the cascade of cytokines. This results in the production of additional inflammatory mediators and further recruitment of immune and inflammatory cells into a joint. Anti–TNF-α treatment strategies (e.g., monoclonal) prevent interaction with receptors on cell surfaces.
The leukotrienes play a major role in the inflammatory response to injury. This class of biologically active molecules has been implicated in the pathogenesis of RA and in other inflammatory diseases (e.g., asthma, psoriasis, inflammatory bowel disease). Leukotrienes are major constituents of a group of oxygenated fatty acids that are synthesized de novo from mem brane phospholipid through a cascade of enzymes. Research studies have focused on these molecules because leukotriene inhibitors and antagonists will probably become important agents in the group of antiinflammatory drugs (see later, “Treatment”).
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