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- W2336804046 abstract "Tumor necrosis factor (TNF)-~ controls T-cell activation and is a major inducer of human immunodeficiency virus (HIV)-I replication in chronically infected cells. Therefore, we have investigated its role in primary cultures of HIV-infected human T lymphocytes by using neutralizing anti-TNF-oL antibodies or TNF-o~. Primary resting T lymphocytes produced TNF-o~ and supported HIV replication after T-cell receptor activation. Addition of neutralizing anti-TNF-ot antibodies drastically reduced p24 antigen release and prevented CD4 + cell depletion associated with infection. Anti-TNF-a also prevented nuclear factor-KB (NF-KB) activation, and a good correlation between this inhibitio n and inhibition of H1V replication was observed. Moreover, supplementing the cultures with high doses of IL-2 reverted anti-TNF-oL inhibition of cell proliferation but did not affect the inhibition of HIV p24 antigen release or NF-KB activation in the same cultures. Moreover, anti-TNF-ot inhibited HIV-1 long terminal repeat (LTR)-driven transcription of a reporter gene in primary T cells in response to activation, either in the presence or the absence of HIV-1 Tat. Our results support an important role for autocrine TNF-o~ secretion in controlling HIV replication in primary T cells because of its ability to maintain NF-KB elevated in the nucleus of T cells. (J Allergy Clin Immunol 1997;100:838-45.)" @default.
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- W2336804046 date "1997-01-01" @default.
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- W2336804046 title "Immunodeficiency and other clinical immunology Replication of human immunodeficiency virus-1 in primary human T cells is dependent on the autocrine secretion of tumor necrosis factor through the control of nuclear factor-KB activation" @default.
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