01870nas a2200361   4500000000100000008004100001260001600042653002700058653002900085653001600114653003100130653001800161653002000179653001400199653003600213653002000249653001700269653001400286653001300300653001100313653001300324653001800337653001600355100001600371700001500387700001300402700001300415245016200428300001200590490000800602520088400610022001401494       1998                            d  c1998 Jun 0110aAntibodies, Monoclonal10aAntigen-Presenting Cells10aCD3 Complex10aCD8-Positive T-Lymphocytes10aCell Division10aCells, Cultured10aCytokines10aCytotoxicity Tests, Immunologic10aDendritic Cells10aEnterotoxins10aFixatives10aGlutaral10aHumans10aMitogens10aSuperantigens10aThalidomide1 aHaslett P A1 aCorral L G1 aAlbert M1 aKaplan G00aThalidomide costimulates primary human T lymphocytes, preferentially inducing proliferation, cytokine production, and cytotoxic responses in the CD8+ subset.  a1885-920 v1873 a<p>The efficacy of thalidomide (alpha-phthalimido-glutarimide) therapy in leprosy patients with erythema nodosum leprosum is thought to be due to inhibition of tumor necrosis factor alpha. In other diseases reported to respond to thalidomide, the mechanism of action of the drug is unclear. We show that thalidomide is a potent costimulator of primary human T cells in vitro, synergizing with stimulation via the T cell receptor complex to increase interleukin 2-mediated T cell proliferation and interferon gamma production. The costimulatory effect is greater on the CD8+ than the CD4+ T cell subset. The drug also increases the primary CD8+ cytotoxic T cell response induced by allogeneic dendritic cells in the absence of CD4+ T cells. Therefore, human T cell costimulation can be achieved pharmacologically with thalidomide, and preferentially in the CD8+ T cell subset.</p>  a0022-1007