CD28 costimulation and T lymphocyte proliferative responses in HIV-1 infection

Clin Exp Immunol. 1997 Sep;109(3):406-11. doi: 10.1046/j.1365-2249.1997.4721370.x.

Abstract

To investigate whether defective costimulatory signals could be involved in the loss of T lymphocyte functions during HIV-1 infection, we tested the effect of CD28 costimulation on both T cell receptor/CD3 and HIV-1 antigen-induced proliferative responses. Although CD3-mediated responses significantly decreased with more advanced stages of HIV-1 infection, the ability of potentiating the responses through CD28 costimulation was maintained at all stages and did not differ from that of HIV-1- subjects. When CD28 costimulation was studied in lymphocyte cultures stimulated with HIV-1 gp160 or p24, potentiation was seen only when a significant response was present without additional CD28 triggering, namely in subjects receiving active immunization with recombinant gp160. These results confirm the integrity of the CD28 pathway of costimulation during HIV-1 infection, and suggest that lymphocytes responding to soluble HIV-1 antigen are not deleted in HIV-1-infected patients, but do not receive significant priming during the natural course of the infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD28 Antigens / immunology*
  • CD3 Complex / immunology
  • Cell Division*
  • Cells, Cultured
  • HIV Core Protein p24 / immunology
  • HIV Envelope Protein gp160 / immunology
  • HIV Infections / immunology*
  • HIV-1*
  • Humans
  • T-Lymphocytes / cytology*
  • T-Lymphocytes / immunology*
  • Vaccination

Substances

  • CD28 Antigens
  • CD3 Complex
  • HIV Core Protein p24
  • HIV Envelope Protein gp160