01972nas a2200301   4500000000100000008004100001260001300042653004200055653001400097653002100111653001000132653001100142653002300153653002800176653002100204653002500225653002500250653001600275653001700291653003200308100001300340245007600353300001000429490000800439050001500447520119400462022001401656       1994                            d  c1994 Oct10aAIDS-Related Opportunistic Infections10aCytokines10aErythema Nodosum10aHIV-110aHumans10aImmunity, Cellular10aInjections, Intradermal10aInterferon-gamma10aLeprosy, lepromatous10aRecombinant Proteins10aThalidomide10aTuberculosis10aTumor Necrosis Factor-alpha1 aKaplan G00aCytokine regulation of disease progression in leprosy and tuberculosis.  a564-80 v191  aKAPLAN19943 a<p>Studies in our laboratory have focussed on the role of cytokines in the regulation of the cellular immune response and disease progression in two important mycobacterial infection of man, namely leprosy and tuberculosis. Our studies in leprosy have involved the use of key regulatory cytokines such as IFN-gamma in the modulation of the cellular response of infected patients. We have investigated the effect of intradermal administration of low dose IFN-gamma on the lesions of anergic lepromatous patients and have reported an accelerated bacillary clearance from the skin. This was associated with the local accumulation of mononuclear cells and killing of infected macrophages. However, IFN-gamma administration also resulted in the induction of erythema nodosum leprosum, a toxic syndrome associated with excess TNF-alpha production. Both the toxic symptoms and the high levels of TNF-alpha production could be inhibited by thalidomide treatment, a drug we have shown reduces the half life of TNF-alpha mRNA. In preliminary clinical trials in tuberculosis patients we have attempted to use thalidomide to reduce TNF-alpha production and toxicities. These results are discussed.</p>  a0171-2985