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Interaction of CD4 with HLA class II antigens and HIV gp120

D Piatier-Tonneau1, L N Gastinel, F Amblard

  • 1Institut d'Embryologie Cellulaire et Moléculaire, CNRS, Collège de France, Nogent-sur-Marne.

Immunogenetics
|January 1, 1991
PubMed

Insights

A new cellular adhesion assay uses B lymphocytes and COS cells to study cell interactions. This assay is specific, quantitative, and inhibited by antibodies and HIV gp120, offering insights into CD4 and HLA class II antigen binding.

Area of Science:

  • Immunology
  • Cell Biology
  • Virology

Background:

  • Cellular adhesion plays a critical role in immune responses.
  • Understanding the interactions between CD4 and HLA class II antigens is crucial for immune cell function.
  • Previous assays for studying these interactions had limitations.

Purpose of the Study:

  • To develop a novel, specific, and quantitative cellular adhesion assay.
  • To investigate the binding interactions between CD4 and HLA class II antigens.
  • To compare the binding sites for HLA class II antigens and HIV gp120 on CD4.

Main Methods:

  • Developed a rosette-based cellular adhesion assay using transfected COS cells expressing CD4 and B lymphocytes expressing HLA class II.
  • Utilized specific antibodies, human immunodeficiency virus (HIV) gp120, and synthetic peptides to inhibit rosette formation.
  • Compared inhibition patterns with other known effector molecules and soluble CD4 derivatives.

Main Results:

  • The assay demonstrated specificity and quantitative measurement of B lymphocyte and COS cell adhesion.
  • Rosette formation was effectively inhibited by CD4- and HLA-DR-specific antibodies and HIV gp120.
  • A synthetic peptide from the HIV gp120 binding site for CD4 also inhibited adhesion, while soluble CD4 derivatives did not.

Conclusions:

  • The developed assay provides a robust method for studying CD4-HLA class II interactions.
  • The findings highlight significant similarities but incomplete identity between CD4 binding sites for HLA class II antigens and HIV gp120.
  • Supports a model of CD4 as an allosteric modulator involved in T-cell adhesion and function, potentially induced by association with the Tcr/CD3 complex.

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