Modulation of TCR usage in HIV-1 infection is regulated by IL-7 and sCD23

Allergol Immunopathol (Madr). 1997 Sep-Oct;25(5):238-46.

Abstract

The purpose of this study is to elucidate the effect of interleukin-7 (IL-7) and soluble CD23 (sCD23) on Phorbol12 Myristate13 Acetate (PMA) activated CD4+ TCR alpha beta+ cells of HIV-1 infected subjects. CD23 and IL-7R were detectable on activated CD4+ T cells of these subjects by FACS. Addition on IL-7 (1000 U/ml), at the onset of cultures, resulted in a significant increase of CD23 expression. We also demonstrated that T cells proliferation and CD23 expression in the presence of exogenous IL-7 occur in an IL-2 independent manner. Addition of IL-7 and sCD23 to activated CD4+ cells of HIV-1 infected subjects induced a proliferative response of TCR alpha beta cells. In contrast, addition of either sCD23 or IL-7 to activated CD4+ T cells did not result in an increase of TCR alpha beta expression. The data provide direct evidence that sCD23 in combination with IL-7 induce proliferation of activated CD4+ T cells of HIV-1 infected subjects to augment TCR alpha beta expression. These results support the possibility that IL-7 plus sCD23 might play an important role in the modulation of TCR alpha beta expression in HIV infection.

MeSH terms

  • Adult
  • Antigens, CD / metabolism
  • CD4-Positive T-Lymphocytes / drug effects
  • CD4-Positive T-Lymphocytes / immunology
  • CD8-Positive T-Lymphocytes / drug effects
  • CD8-Positive T-Lymphocytes / immunology
  • HIV Infections / immunology*
  • Humans
  • Interleukin-7 / pharmacology*
  • Lymphocyte Activation
  • Male
  • Receptors, Antigen, T-Cell, alpha-beta / drug effects*
  • Receptors, IgE / metabolism*
  • Receptors, Interleukin / metabolism
  • Receptors, Interleukin-7
  • Tetradecanoylphorbol Acetate / pharmacology

Substances

  • Antigens, CD
  • Interleukin-7
  • Receptors, Antigen, T-Cell, alpha-beta
  • Receptors, IgE
  • Receptors, Interleukin
  • Receptors, Interleukin-7
  • Tetradecanoylphorbol Acetate