Anti-phospholipid human monoclonal antibodies inhibit CCR5-tropic HIV-1 and induce beta-chemokines

J Exp Med. 2010 Apr 12;207(4):763-76. doi: 10.1084/jem.20091281. Epub 2010 Apr 5.

Abstract

Traditional antibody-mediated neutralization of HIV-1 infection is thought to result from the binding of antibodies to virions, thus preventing virus entry. However, antibodies that broadly neutralize HIV-1 are rare and are not induced by current vaccines. We report that four human anti-phospholipid monoclonal antibodies (mAbs) (PGN632, P1, IS4, and CL1) inhibit HIV-1 CCR5-tropic (R5) primary isolate infection of peripheral blood mononuclear cells (PBMCs) with 80% inhibitory concentrations of <0.02 to approximately 10 microg/ml. Anti-phospholipid mAbs inhibited PBMC HIV-1 infection in vitro by mechanisms involving binding to monocytes and triggering the release of MIP-1alpha and MIP-1beta. The release of these beta-chemokines explains both the specificity for R5 HIV-1 and the activity of these mAbs in PBMC cultures containing both primary lymphocytes and monocytes.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Antibodies, Antiphospholipid / genetics
  • Antibodies, Antiphospholipid / immunology
  • Antibodies, Antiphospholipid / pharmacology*
  • Antibodies, Monoclonal / genetics
  • Antibodies, Monoclonal / immunology
  • Antibodies, Monoclonal / pharmacology*
  • CD4-Positive T-Lymphocytes / drug effects
  • CD4-Positive T-Lymphocytes / virology
  • Cardiolipins / immunology
  • Cell Fusion
  • Chemokine CCL3 / immunology
  • Chemokine CCL3 / metabolism
  • Chemokine CCL4 / immunology
  • Chemokine CCL4 / metabolism
  • Chemokines / metabolism
  • Chemokines, CC / metabolism*
  • Complementarity Determining Regions / genetics
  • Culture Media, Conditioned / pharmacology
  • Endotoxins / pharmacology
  • Epithelial Cells / virology
  • Giant Cells / cytology
  • HIV-1 / classification
  • HIV-1 / physiology*
  • Humans
  • Immunity, Innate / drug effects
  • Immunity, Innate / immunology
  • Immunoglobulin Fab Fragments / genetics
  • Immunoglobulin Fab Fragments / immunology
  • Immunoglobulin Fc Fragments / immunology
  • Kinetics
  • Leukocytes, Mononuclear / drug effects
  • Leukocytes, Mononuclear / immunology
  • Leukocytes, Mononuclear / virology
  • Monocytes / drug effects
  • Monocytes / immunology
  • Monocytes / metabolism
  • Monocytes / virology
  • Mutation / genetics
  • Mutation / immunology
  • Phosphatidylethanolamines / immunology
  • Phosphatidylserines / immunology
  • Receptors, CCR5 / physiology*
  • Viral Tropism / physiology*
  • Virus Internalization / drug effects*
  • beta 2-Glycoprotein I / immunology
  • env Gene Products, Human Immunodeficiency Virus / immunology
  • env Gene Products, Human Immunodeficiency Virus / metabolism

Substances

  • 1,2-dioleoyl-glycero-3-phosphatidyl ethanolamine
  • Antibodies, Antiphospholipid
  • Antibodies, Monoclonal
  • CCL3 protein, human
  • CCL4 protein, human
  • Cardiolipins
  • Chemokine CCL3
  • Chemokine CCL4
  • Chemokines
  • Chemokines, CC
  • Complementarity Determining Regions
  • Culture Media, Conditioned
  • Endotoxins
  • Immunoglobulin Fab Fragments
  • Immunoglobulin Fc Fragments
  • Phosphatidylethanolamines
  • Phosphatidylserines
  • Receptors, CCR5
  • beta 2-Glycoprotein I
  • env Gene Products, Human Immunodeficiency Virus