01906nas a2200301   4500000000100000008004100001260001300042653001400055653001400069653002100083653001100104653002900115653001900144653001400163653002500177653001900202653001600221653003200237100001600269700001800285700001700303700001400320245013800334300000900472490000700481520110200488022001401590       2002                            d  c2002 Feb10aApoptosis10aCytokines10aErythema Nodosum10aHumans10aImmunosuppressive Agents10aInterleukin-1210aMonocytes10aMycobacterium leprae10aRNA, Messenger10aThalidomide10aTumor Necrosis Factor-alpha1 aSampaio E P1 aHernandez M O1 aCarvalho D S1 aSarno E N00aManagement of erythema nodosum leprosum by thalidomide: thalidomide analogues inhibit M. leprae-induced TNFalpha production in vitro.  a13-90 v563 a<p>Thalidomide is being successfully used for the treatment of erythema nodosum leprosum (ENL), among other disorders with inflammatory and immunological bases. Although the active molecules responsible for the diverse therapeutic activities of the drug and the sequence of reactions triggered inside the cells remain unclear, it was demonstrated that thalidomide (THAL) inhibits TNFalpha mRNA expression and protein production by stimulated monocytes and activated T lymphocytes. Patients treated with THAL experienced a reduction in serum TNFalpha levels and it diminished cytokine gene expression at the lesion site, with a concomitant abrogation of clinical symptoms. It has been reported that thalidomide as well as some its analogues decrease M. leprae-induced TNFalpha and IL-12 mRNA in vitro. THAL also reduced monocyte apoptosis in the cultures. The present data further support thalidomide's effects on TNFa synthesis and the growing need to search for new specific TNFalpha inhibitors (non-teratogenic compounds) that might be potentially used in clinical disorders such as leprosy.</p>  a0753-3322