Th2-like CD8+ T cells showing B cell helper function and reduced cytolytic activity in human immunodeficiency virus

E Maggi1, M G Giudizi, R Biagiotti

  • 1Division of Clinical Immunology and Allergy, University of Florence, Italy.

Insights

Human immunodeficiency virus type 1 (HIV-1) infection can cause T cells to switch from cytotoxic to cytokine-producing cells. This shift may explain immune deficiency and allergic symptoms in patients.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • HIV-1 infection severely impacts T lymphocyte populations, particularly CD4+ T cells.
  • Some HIV-1 patients exhibit Job's-like syndrome with eczema, recurrent infections, and high IgE levels, despite low CD4+ T cell counts.

Purpose of the Study:

  • To investigate the functional profile of T lymphocytes at a clonal level in HIV-1 infected individuals with Job's-like syndrome.
  • To understand the cellular mechanisms underlying immune dysfunction and allergic manifestations in these patients.

Main Methods:

  • Clonal analysis of circulating and skin-infiltrating T lymphocytes from two HIV-1 infected patients.
  • Characterization of T cell surface markers (CD4, CD8, TCR alpha beta), cytokine production (IFN-gamma, IL-4, IL-5), and cytolytic activity.
  • Assessment of B cell helper function for IgE synthesis.

Main Results:

  • Most T cell clones from patients were CD4- CD8+ or CD4- CD8-.
  • These T cells exhibited reduced interferon-gamma production and cytolytic activity.
  • A majority produced interleukin-4 and interleukin-5, providing B cell help for IgE synthesis.

Conclusions:

  • HIV-1 infection can induce a switch in CD8+ T cells from a cytotoxic (Th1-like) to a cytokine-producing (Th2-like) phenotype.
  • This T cell functional shift may contribute to impaired defense against infections and allergic-like symptoms, including elevated IgE.
  • The findings offer insights into the complex immune dysregulation observed in certain HIV-1 infected individuals.

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