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lüll HIV-1 immunopathogenesis: how good interferon turns bad Herbeuval JP; Shearer GMClin Immunol 2007[May]; 123 (2): 121-8The hallmark of acquired immunodeficiency syndrome (AIDS) is the progressive loss of CD4+ T cells that results from infection with human immunodeficiency virus type-1 (HIV-1). Despite 25 years of AIDS research, questions remain concerning the mechanisms responsible for HIV-induced CD4+ T cell depletion. Here we briefly review the in vitro and in vivo literature concerning the protective role of interferon-alpha (IFN-alpha) in HIV/AIDS. We then develop a laboratory- and clinically supported model of CD4+ T cell apoptosis in which either infectious or noninfectious HIV-1 induces the production of type I interferon by plasmacytoid dendritic cells (pDC). The interferon produced binds to its receptor on primary CD4+ T cells resulting in membrane expression of the TNF-related apoptosis-inducing ligand (TRAIL) death molecule. The binding of infectious or noninfectious HIV-1 to CD4 on these T cells results in expression of the TRAIL death receptor 5 (DR5), leading to the selective death of HIV-exposed CD4+ T cells.|Apoptosis/immunology[MESH]|CD4-Positive T-Lymphocytes/immunology/metabolism/virology[MESH]|Dendritic Cells/immunology/metabolism/virology[MESH]|HIV Infections/etiology/*immunology/metabolism[MESH]|HIV-1/*immunology[MESH]|Humans[MESH]|Interferon-alpha/*metabolism[MESH]|Models, Biological[MESH]|Receptors, TNF-Related Apoptosis-Inducing Ligand/metabolism[MESH]|TNF-Related Apoptosis-Inducing Ligand/metabolism[MESH] |