TY - JOUR
T1 - Transforming growth factor β suppresses human immunodeficiency virus expression and replication in infected cells of the monocyte/macrophage lineage
AU - Poli, Guido
AU - Kinter, Audrey L.
AU - Justement, Jesse S.
AU - Bressler, Peter
AU - Kehrl, John H.
AU - Fauci, Anthony S.
PY - 1991
Y1 - 1991
N2 - The pleiotropic immunoregulatory cytokine transforming growth factor β (TGF-β) potently suppresses production of the human immunodeficiency virus (HIV), the causative agent of the acquired immunodeficiency syndrome, in the chronically infected promonocytic cell line U1. TGF-β significantly (50-90%) inhibited HIV reverse transcriptase production and synthesis of viral proteins in U1 cells stimulated with phorbol myristate acetate (PMA) or interleukin 6 (IL-6). Furthermore, TGF-β suppressed PMA induction of HIV transcription in U1 cells. In contrast, TGF-β did not significantly affect the expression of HIV induced by tumor necrosis factor α (TNF-α). These suppressive effects were not mediated via the induction of interferon a (IFN-α). TGF-β also suppressed HIV replication in primary monocyte-derived macrophages infected in vitro, both in the absence of exogenous cytokines and in IL-6-stimulated cultures. In contrast, no significant effects of TGF-β were observed in either a chronically infected T cell line (ACH-2) or in primary T cell blasts infected in vitro. Therefore, TGF-β may play a potentially important role as a negative regulator of HIV expression in infected monocytes or tissue macrophages in infected individuals.
AB - The pleiotropic immunoregulatory cytokine transforming growth factor β (TGF-β) potently suppresses production of the human immunodeficiency virus (HIV), the causative agent of the acquired immunodeficiency syndrome, in the chronically infected promonocytic cell line U1. TGF-β significantly (50-90%) inhibited HIV reverse transcriptase production and synthesis of viral proteins in U1 cells stimulated with phorbol myristate acetate (PMA) or interleukin 6 (IL-6). Furthermore, TGF-β suppressed PMA induction of HIV transcription in U1 cells. In contrast, TGF-β did not significantly affect the expression of HIV induced by tumor necrosis factor α (TNF-α). These suppressive effects were not mediated via the induction of interferon a (IFN-α). TGF-β also suppressed HIV replication in primary monocyte-derived macrophages infected in vitro, both in the absence of exogenous cytokines and in IL-6-stimulated cultures. In contrast, no significant effects of TGF-β were observed in either a chronically infected T cell line (ACH-2) or in primary T cell blasts infected in vitro. Therefore, TGF-β may play a potentially important role as a negative regulator of HIV expression in infected monocytes or tissue macrophages in infected individuals.
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M3 - Article
C2 - 1705278
AN - SCOPUS:0026026407
VL - 173
SP - 589
EP - 597
JO - Journal of Experimental Medicine
JF - Journal of Experimental Medicine
SN - 0022-1007
IS - 3
ER -