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[Cytotoxic response against human immunodeficiency virus (HIV): control with suppressor factor]

B Sadat-Sowti1, P Debré, B Autran

  • 1Laboratoire d'Immunologie tissulaire et cellulaire, CERVI, Paris.

Comptes Rendus Des Seances De La Societe De Biologie Et De Ses Filiales
|January 1, 1992
PubMed

Insights

CD8+ CD57+ lymphocytes from HIV patients suppress immune cell activity. This inhibition is caused by a unique soluble glycoprotein, not previously identified factors.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Human Immunodeficiency Virus (HIV) infection alters immune cell function.
  • CD8+ CD57+ lymphocytes are implicated in immune regulation.
  • The precise mechanisms of immune suppression in HIV are not fully understood.

Purpose of the Study:

  • To investigate the suppressor function of CD8+ CD57+ lymphocytes in HIV-seropositive patients.
  • To characterize the nature of the inhibitory factor produced by these lymphocytes.

Main Methods:

  • Isolation and characterization of CD8+ CD57+ lymphocytes from HIV-seropositive patients.
  • Assay of the cytolytic activity of allospecific cytotoxic T lymphocytes (CTL), natural killer (NK), and lymphokine-activated killer (LAK) cells.
  • Biochemical analysis of the soluble inhibitory factor, including heat, trypsin, and pronase E resistance, and concanavalin A-sepharose binding.

Main Results:

  • CD8+ CD57+ lymphocytes from HIV-seropositive patients exhibit a suppressor function.
  • This suppression inhibits the cytolytic activity of allospecific CTL, NK, and LAK cells.
  • The inhibitory effect is mediated by a soluble factor distinct from PGE2, TGF-β, TNF-α, and TNF-β.
  • The factor is heat and trypsin resistant, sensitive to pronase E, binds to concanavalin A-sepharose, and has a molecular weight of 20-30 kDa, indicating it is a glycoprotein.

Conclusions:

  • A novel suppressor function of CD8+ CD57+ lymphocytes in HIV infection has been identified.
  • A unique glycoprotein mediates this non-antigen-specific immunosuppression.
  • Understanding this mechanism could offer new therapeutic targets for HIV-associated immune dysfunction.

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