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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

  • Krystyna Konopka
  • Brian R. Davis
  • Nejat Düzgüneş
Part of the Advances in Experimental Medicine and Biology book series (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).

Keywords

Human Immunodeficiency Virus Human Immunodeficiency Virus Type Simian Immunodeficiency Virus Large Unilamellar Vesicle Antigen Receptor Complex 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1991

Authors and Affiliations

  • Krystyna Konopka
    • 1
  • Brian R. Davis
    • 3
  • Nejat Düzgüneş
    • 1
    • 2
    • 4
  1. 1.Cancer Research InstituteUniversity of CaliforniaSan FranciscoUSA
  2. 2.Department of Pharmaceutical ChemistryUniversity of CaliforniaSan FranciscoUSA
  3. 3.Medical Research Institute of San Francisco at Pacific Presbyterian Medical CenterSan FranciscoUSA
  4. 4.Department of MicrobiologyUniversity of the Pacific, School of DentistrySan FranciscoUSA

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