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In Vitro Assay to Evaluate the Impact of Immunoregulatory Pathways on HIV-specific CD4 T Cell Effector Function
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Published on: October 16, 2013

Recombinant human IL-16 inhibits HIV-1 replication and protects against activation-induced cell death (AICD)

T Idziorek1, J Khalife, O Billaut-Mulot

  • 1Institut Pasteur de Lille, INSERM U167, France.

Clinical and Experimental Immunology
|May 5, 1998
PubMed

Insights

Interleukin-16 (IL-16) reduces apoptosis in activated T cells from HIV-1 patients. This cytokine

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Interleukin-16 (IL-16) is a chemoattractant cytokine with known effects on lymphocyte activation and HIV-1 replication.
  • Recombinant human IL-16 was produced in E. coli to study its effects on lymphocyte apoptosis in HIV-1 infection.

Purpose of the Study:

  • To investigate the potential of recombinant IL-16 to regulate lymphocyte apoptosis in HIV-1-infected individuals.
  • To explore the mechanism by which IL-16 might influence apoptosis, specifically its effect on CD95 expression.

Main Methods:

  • Cloning and expression of human IL-16 in Escherichia coli.
  • Purification and refolding of recombinant IL-16.
  • Assessing lymphocyte apoptosis in peripheral blood mononuclear cell (PBMC) cultures from HIV-1-infected subjects and healthy individuals under various stimulation conditions (anti-CD3, anti-CD95, dexamethasone).
  • Measuring CD95 expression on activated CD4+ T cells.

Main Results:

  • Bacterially derived recombinant IL-16 required high concentrations for significant HIV-1 replication inhibition, likely due to low yields of the active homotetrameric form.
  • IL-16 did not affect spontaneous lymphocyte apoptosis in unstimulated PBMCs from HIV-1-infected subjects.
  • IL-16 significantly reduced activation-induced cell death (AICD) in PBMCs stimulated with anti-CD3, anti-CD95, or dexamethasone.
  • The reduction in AICD correlated with decreased CD95 expression on activated CD4+ T cells.
  • IL-16's regulation of apoptosis is complex and may depend on the stimulus and lymphocyte immune status.

Conclusions:

  • Recombinant IL-16 demonstrates a capacity to inhibit activation-induced cell death in lymphocytes from HIV-1-infected individuals.
  • The anti-apoptotic effect of IL-16 is linked to its ability to downregulate CD95 expression on activated CD4+ T cells.
  • IL-16 shows potential therapeutic value in managing HIV disease by modulating lymphocyte apoptosis and immune cell activation.

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