Decreased accessory cell function by human monocytic cells after infection with HIV

J Immunol. 1988 Mar 1;140(5):1485-9.

Abstract

We studied the effect of HIV infection on the human monocytic cell line U937. The cell line was infected with cellfree HIV, strain HTLV-IIIB. After 3 wk, a high reverse transcriptase activity was continuously detected in the supernatant of the cell line. Neither cytopathic effects nor changes in cell growth were observed. After infection, accessory cell function on T cell proliferation induced by anti-CD3 mAb of both IgG1 and IgG2a subclasses and Con A was tested. Accessory cell function provided by U937 cells started to decline 3 wk after inoculation with HIV. This correlated with detectable reverse transcriptase activity. The remaining accessory cell capacity varied between 10 and 60% of accessory cell function mediated by noninfected U937 cells. It was excluded that decreased FcR expression on U937/HIV cells contributed to the accessory cell defect in the anti-CD3-driven system. IL-2R expression on T cells, cocultivated with U937/HIV and anti-CD3, was minimal. The accessory cell defect could only be partly overcome by addition of rIL-2 or IL-1. Addition of high titer (10(4) TCID50) HIV or U937/HIV cells did not affect T cell proliferation, which rules out that the observed inhibition is caused by HIV infection of T cells or suppressive effects of U937/HIV cells. These results suggest that infection of APC may contribute to the induction of immunologic abnormalities in early HIV infection. Thus, monocytes/macrophages may not only serve as a reservoir for the dissemination of HIV, but may be an important target cell through which the immune system is affected.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acquired Immunodeficiency Syndrome / immunology*
  • Antigen-Presenting Cells / immunology*
  • Antigens, Differentiation, T-Lymphocyte / immunology
  • Cell Line
  • Humans
  • Immune Sera / pharmacology
  • Immunosuppression Therapy*
  • Interleukin-1 / pharmacology
  • Interleukin-2 / metabolism
  • Interleukin-2 / pharmacology
  • Lymphocyte Activation
  • Monocytes / immunology*
  • Monocytes / microbiology
  • Receptors, Fc / analysis
  • Receptors, IgG
  • Receptors, Immunologic / biosynthesis
  • Receptors, Interleukin-2
  • Recombinant Proteins / pharmacology
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism

Substances

  • Antigens, Differentiation, T-Lymphocyte
  • Immune Sera
  • Interleukin-1
  • Interleukin-2
  • Receptors, Fc
  • Receptors, IgG
  • Receptors, Immunologic
  • Receptors, Interleukin-2
  • Recombinant Proteins