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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-06-02
    Description: Cell fusion (syncytium formation) is a major cytopathic effect of infection by human immunodeficiency virus (HIV) and may also represent an important mechanism of CD4+ T-cell depletion in individuals infected with HIV. Syncytium formation requires the interaction of CD4 on the surface of uninfected cells with HIV envelope glycoprotein gp120 expressed on HIV-infected cells. However, several observations suggest that molecules other than CD4 play a role in HIV-induced cell fusion. The leukocyte adhesion receptor LFA-1 is involved in a broad range of leukocyte interactions mediated by diverse receptor-ligand systems including CD4-class II major histocompatibility complex (MHC) molecules. Possible mimicry of class II MHC molecules by gp120 in its interaction with CD4 prompted an examination of the role of LFA-1 in HIV-induced cell fusion. A monoclonal antibody against LFA-1 completely inhibited HIV-induced syncytium formation. The antibody did not block binding of gp120 to CD4. This demonstrates that a molecule other than CD4 is also involved in cell fusion mediated by HIV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hildreth, J E -- Orentas, R J -- 5T32CA09243/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 2;244(4908):1075-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2543075" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Antigens, Differentiation/immunology/*physiology ; Antigens, Differentiation, T-Lymphocyte/immunology ; Cell Fusion ; Cell Line ; Cytopathogenic Effect, Viral ; HIV/immunology/*physiology ; HIV Envelope Protein gp120 ; Histocompatibility Antigens Class II/immunology ; Humans ; Lymphocyte Function-Associated Antigen-1 ; Phytohemagglutinins/pharmacology ; Retroviridae Proteins/immunology ; T-Lymphocytes/immunology/*microbiology ; Viral Envelope Proteins/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 1990-06-08
    Description: Cytolytic T lymphocyte (CTL) responses were evaluated in humans immunized with recombinant human immunodeficiency virus type 1 (HIV) envelope glycoprotein gp160. Some vaccinees had gp160-specific CTLs that were shown by cloning to be CD4+. Although induced by exogenous antigen, most gp160-specific CTL clones also recognized gp160 synthesized endogenously in target cells. These clones lysed autologous CD4+ T lymphoblasts infected with HIV. Of particular interest were certain vaccine-induced clones that lysed HIV-infected cells, recognized gp160 from diverse HIV isolates, and did not participate in "innocent bystander" killing of noninfected CD4+ T cells that had bound gp120.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Orentas, R J -- Hildreth, J E -- Obah, E -- Polydefkis, M -- Smith, G E -- Clements, M L -- Siliciano, R F -- 5T32CA09243/CA/NCI NIH HHS/ -- AI28108/AI/NIAID NIH HHS/ -- N01AI62515/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Jun 8;248(4960):1234-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2190315" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Clone Cells ; Cytotoxicity, Immunologic ; Gene Products, env/*immunology ; HIV/*immunology ; HIV Envelope Protein gp160 ; HIV Seropositivity ; Humans ; Immunization ; Macromolecular Substances ; Protein Precursors/*immunology ; Recombinant Proteins/immunology ; T-Lymphocytes, Cytotoxic/*immunology ; Viral Vaccines/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 1990-07-27
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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