The mechanism of action of thalidomide is not completely understood. In vitro and in vivo studies indicate that it inhibits the production of tumor necrosis factor-alpha in monocytes. Thalidomide may induce the down regulation of integrin receptors and other surface adhesion proteins, reduce IgM production, alter CD4/CD8 T-cell ratios as well as increase the total numbers of CD8 and CD4 T-cells, and inhibit angiogenesis. Anti-inflammatory properties have been suggested through decreasing the production of oxygen-free radicals and other mediators in inflammatory response. Thalidomide may enhance cell-mediated immunity by directly stimulating cytotoxic T-cells.