HIV and Rheumatological Disease

A probable role for mast cells and IgE-mediated pathology has been reported in HIV infection (130). The chemokine receptor, CCR3 is expressed on mast cells and may provide one explanation for the chemotactic effects of tat protein on mast cells (130). In one study, increased adventitial mast cell numbers were noted in the arteries of patients dying of cocaine toxicity (131,132), but the role of mast cells in HIV and cocaine-induced vascular pathology is unclear (132).

Mast cells may play a role in various arthritides. For example, the release of mast cell mediators (a- and P-tryptase and histamine) has been demonstrated in the joint of various forms of inflammatory arthritis (133,134). In osteoar-thritis, a degenerative but potentially inflammatory disorder, mast cell counts and tryptase and histamine levels are elevated in synovial fluid (135,136). Activated mast cells also are seen in the lesions present in patients with rheumatoid arthritis (137-139), whereas mast cell chemotactic activity and their expression of VEGF have been demonstrated in rheumatoid synovium (140,141). Mast cell infiltration of the minor salivary glands is observed in patients with Sjogren's syndrome, and this infiltration often is associated with fibrosis and c-kit expression (142). Patients with fibromyalgia demonstrate higher dermal deposits of IgG and increased dermal mast cell numbers, but the role these play in pathogenesis of the disease is unknown (143).

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