The effects of IL-13 on monocytes/macrophages and endothelial cells are similar to those of IL-4. IL-1 } modulates the phenotype of both human and murine monocytes/macrophages and it inhibits production of proinflammatory cytokines, chemokines and nitric-oxide by these cells. IL-13 inhibits synthesis of IL-la, IL-1 p, IL-6, IL-12, tumor necrosis factor a (TNE-a) and the chemokines IL-8, macrophage inflammatory protein (MlP-la) and MIP-1|3 by monocytes. In addition, it enhances production of the IL-1 receptor antagonist, which is a secreted protein with antiinflammatory properties. IL-13 also inhibits IL-1 (3 and TNFa production by synovial fluid macrophages from patients with rheumatoid arthritis, suggesting that IL-13 may have therapeutic potential in the treatment of inflammatory arthritis. This notion is supported by the observation that IL-13-producing cells attenuate collagen-induced arthritis in mice. IL-13 was also shown to suppress experimental autoimmune encephalomyelitis in rats, further demonstrating its anti-inflammatory properties in vivo. In addition, IL-13 enhances expression of CD lib, CDllc, CD18, CD23 and MHC class II molecules, whereas it decreases expression of CD 14, CD 16, CD32 and CD64 on monocytes and macrophages.
IL-13 induces VCAM-1 expression on human umbilical vein endothelial cells, which results in adhesion of eosinophils to these cells. Eosinophils accumulate at sites of allergic inflammation, and they are thought to play a crucial role in the pathogenesis of the lung inflammation and in lung epithelial cell destruction in asthmatic patients. Consequently, the ability of IL-13, like that of IL-4, to induce VCAM-1 expression on endothelial cells further emphasizes the importance of these cytokines in the pathogenesis of allergic and asthmatic responses.
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