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New Tools to Expand Regulatory T Cells from HIV-1-infected Individuals
Published on: May 30, 2013
[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
Summary
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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