Linked Life Data

16524887

Source:http://linkedlifedata.com/resource/pubmed/id/16524887

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pubmed-article:16524887pubmed:abstractTextThe molecular mechanism of the human immunodeficiency virus type 1 (HIV-1) gp120-induced apoptosis of bystander T cells is not well defined. Here, we demonstrate that CD45, a key component of the T cell receptor pathway, plays a crucial role in apoptosis induced by HIV-1 gp120. We observed that HIV-1 gp120-induced apoptosis was significantly reduced in a CD45-deficient cell line and that reconstitution of CD45 in these cells restored gp120-induced apoptosis. However, expression of a chimeric protein containing only the intracellular phosphatase domain was not able to restore the apoptotic function in the CD45-negative clone, indicating an important role for the extracellular domain of CD45 in this function. The role of CD45 in gp120-induced apoptosis was further confirmed in T cell lines and peripheral blood mononuclear cells using a selective CD45 inhibitor as well as CD45-specific small interfering RNA. We also observed that gp120 treatment induced CD45 association with the HIV coreceptor CXCR4. Further elucidation of downstream signaling events revealed that CD45 modulates HIV-1 gp120-induced apoptosis by regulating Fas ligand induction and activation of the phosphoinositide 3-kinase/Akt pathway. These results suggest a novel CD45-mediated mechanism for the HIV envelope-induced apoptosis of T cells.lld:pubmed
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pubmed-article:16524887pubmed:dateRevised2010-11-18lld:pubmed
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pubmed-article:16524887pubmed:articleTitleHIV-1 gp120-mediated apoptosis of T cells is regulated by the membrane tyrosine phosphatase CD45.lld:pubmed
pubmed-article:16524887pubmed:affiliationDivision of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA.lld:pubmed
pubmed-article:16524887pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:16524887pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
pubmed-article:16524887pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
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