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pubmed-article:9819674pubmed:abstractTextIn humans, tuberculosis is associated with suppression of T-cell responses to antigens of Mycobacterium tuberculosis. Recently, the macrophage product, transforming growth factor-beta (TGF-beta) has been implicated in suppression of T-cell proliferation and cytokine production during tuberculosis. We studied the effect of TGF-beta on production of IL-12, and on the augmentation of M. tuberculosis-induced IFN gamma production by IL-12, in patients with pulmonary tuberculosis and by M. tuberculosis. Induction of IL-12 p35, but not IL-12 p40, by M. tuberculosis in monocytes was dependent on prior priming of the cells with IFN gamma. Expression of both IL-12 p40 and p35, however, was suppressed by TGF-beta. Further, TGF-beta interfered with the bioactivity of IL-12 in the enhancement of M. tuberculosis-induced IFN gamma mRNA expression and cytokine production. However, in mononuclear cells from patients with tuberculosis the main effect of TGF-beta on IL-12 appeared to be counter action to IL-12 induced IFN gamma production in response to M. tuberculosis.lld:pubmed
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pubmed-article:9819674pubmed:pagination59-75lld:pubmed
pubmed-article:9819674pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:9819674pubmed:articleTitleModulation of IL-12 by transforming growth factor-beta (TGF-beta) in Mycobacterium tuberculosis-infected mononuclear phagocytes and in patients with active tuberculosis.lld:pubmed
pubmed-article:9819674pubmed:affiliationDivision of Infectious Diseases, Case Western Reserve University, Cleveland, Ohio 44106, USA. zxt2@pocwruedulld:pubmed
pubmed-article:9819674pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:9819674pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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