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HIV-1 Infection of a Non-CD4-Expressing Variant of HUT-78 Cells: Lack of Inhibition by LEU3A Antibodies and Enhancement by Cationic DOTMA Liposomes

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Mechanisms and Specificity of HIV Entry into Host Cells

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 300))

Abstract

CD4 and CD8 are membrane glycoproteins that have been implicated in recognition of MHC class-II (HLA-DR, DQ, DP and I-A/I-E) and class-I (HLA-A,B, C and H-2) antigens, respectively. CD4 and CD8 are expressed on functionally distinct populations of mature peripheral T lymphocytes; CD4 on helper/inducer cells and CD8 on cytotoxic/supressor cells (Reinherz and Schlossman, 1980). The CD4 molecule is expressed as a monomer on the cell surface of T lymphocytes and some cells of the macrophage/monocytes lineage, and is a transmembrane glycoprotein of ̃ 55 kD with homology to members of the immunoglobulin (Ig) supergene family. It has four external 1g variable-like domains (V1 - V4), one transmembrane domain and a cytoplasmic tail of 40 residues (Maddon et al, 1985). The precise role of the CD4 molecule in T cell function is unknown. It has been proposed that CD4 may increase the avidity of the T cell receptor (TcR) for its ligand(s) by directly binding to monomorphic determinants of class II MHC molecules on target cells. Transfection of a cDNA encoding the human CD4 molecule into antigen-responsive T-cell hybridomas greatly enhanced the cells’ responsiveness to antigenic stimulation (Doyle and Strominger, 1987; Gay et al., 1987; Sleckman et al., 1987). In addition, CD4 may associate with the TcR as part of the antigen recognition process (Janeway et al.,1987; Saizawa et al, 1987) and may be directly involved in the resultant signal transduction (Emmerich et al., 1987; Carrel et al., 1988), possibly in concert with a lymphocyte-specific protein tyrosine kinase (reviewed by Robey and Axel, 1990).

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Authors and Affiliations

  1. Cancer Research Institute, University of California, San Francisco, California, 94143, USA

    Krystyna Konopka & Nejat Düzgüneş

  2. Department of Pharmaceutical Chemistry, University of California, San Francisco, California, 94143, USA

    Nejat Düzgüneş

  3. Medical Research Institute of San Francisco at Pacific Presbyterian Medical Center, San Francisco, CA, 94115, USA

    Brian R. Davis

  4. Department of Microbiology, University of the Pacific, School of Dentistry, San Francisco, CA, 94115, USA

    Nejat Düzgüneş

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  1. Krystyna Konopka
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  2. Brian R. Davis
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  3. Nejat Düzgüneş
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Editors and Affiliations

  1. University of the Pacific, San Francisco, California, USA

    Nejat Düzgüneş

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© 1991 Plenum Press, New York

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Konopka, K., Davis, B.R., Düzgüneş, N. (1991). HIV-1 Infection of a Non-CD4-Expressing Variant of HUT-78 Cells: Lack of Inhibition by LEU3A Antibodies and Enhancement by Cationic DOTMA Liposomes. In: Düzgüneş, N. (eds) Mechanisms and Specificity of HIV Entry into Host Cells. Advances in Experimental Medicine and Biology, vol 300. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5976-0_7

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  • DOI: https://doi.org/10.1007/978-1-4684-5976-0_7

  • Publisher Name: Springer, Boston, MA

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