HIV type 1-induced inhibition of CD45 tyrosine phosphatase activity correlates with disease progression and apoptosis, but not with anti-CD3-induced T cell proliferation

AIDS Res Hum Retroviruses. 2000 Feb 10;16(3):211-9. doi: 10.1089/088922200309304.

Abstract

The tyrosine phosphatase CD45 is a key positive element in multiple lymphocyte signaling pathways. To understand the contribution of CD45 to HIV-1-induced T cell hyporesponsiveness and apoptosis we evaluated the CD45-associated tyrosine phosphatase activity of lymphocytes from patients with different stages of HIV-1 disease and compared it with CD45 expression, spontaneous and Fas-induced apoptosis, anti-CD3-induced T cell proliferation, distribution of CCR5 delta32/wt, and cytokine production. The proliferative response to anti-CD3 as well as the CD45-associated phosphatase activity were significantly reduced in progressors. In long-term nonprogressors (LTNPs) the proliferative response to anti-CD3 was also diminished, although to a lesser extent, while the tyrosine phosphatase activity was not significantly impaired. One-third of LTNPs were found positive for the 32-bp deletion of the CCR5 gene. This mutation had no effects on anti-CD3 proliferative response or CD45 phosphatase activity. A significant reduction in IL-2 and IFN-gamma was observed in both LTNPs and in normal progressors, whereas IL-4 production was significantly decreased only in progressors. Last, we observed a significant correlation between CD45 phosphatase activity and apoptosis. We therefore conclude that the impairment of CD45 tyrosine phosphatase activity correlates with disease progression and the level of T cell apoptosis, but not with anti-CD3-induced T cell proliferation. Moreover, we suggest that evaluation of CD45 tyrosine phosphatase activity may represent an additional tool with which to assess disease progression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Apoptosis / immunology*
  • CD3 Complex / immunology
  • Cell Division
  • Cells, Cultured
  • Disease Progression
  • HIV Infections / blood
  • HIV Infections / enzymology*
  • HIV Infections / immunology
  • HIV Infections / physiopathology
  • HIV-1 / metabolism*
  • HIV-1 / physiology
  • Humans
  • Interferon-gamma / biosynthesis
  • Interleukin-2 / biosynthesis
  • Interleukin-4 / biosynthesis
  • Leukocyte Common Antigens / metabolism*
  • Lymphocyte Activation
  • Middle Aged
  • Mutagenesis
  • Protein Tyrosine Phosphatase, Non-Receptor Type 1
  • Receptors, CCR5 / genetics
  • T-Lymphocytes / enzymology*
  • T-Lymphocytes / immunology
  • fas Receptor / immunology

Substances

  • CD3 Complex
  • Interleukin-2
  • Receptors, CCR5
  • fas Receptor
  • Interleukin-4
  • Interferon-gamma
  • Leukocyte Common Antigens
  • Protein Tyrosine Phosphatase, Non-Receptor Type 1