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Related Experiment Videos

Trypanosoma cruzi-induced decrease in the level of interferon-gamma receptor expression by resting and activated

F Kierszenbaum1, H Mejia Lopez, M K Tanner

  • 1Department of Microbiology, Michigan State University, East Lansing 44824, USA.

Parasite Immunology
|April 1, 1995
PubMed
Summary

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Trypanosoma cruzi infection significantly reduces interferon-gamma receptor (IFN-gamma R) expression on human B cells. This suppression, caused by parasite components, suggests impaired immune signaling during infection.

Area of Science:

  • Immunology
  • Cell Biology
  • Parasitology

Background:

  • Interferon-gamma receptors (IFN-gamma R) are crucial for immune cell activation.
  • Trypanosoma cruzi (T. cruzi) is a parasite that causes Chagas disease.
  • Dysregulation of immune cell surface receptors can impair host defense.

Purpose of the Study:

  • To investigate the effect of T. cruzi on IFN-gamma R expression in human peripheral blood mononuclear cells (PBMCs).
  • To identify which lymphocyte subsets are most affected by T. cruzi co-culture.
  • To explore the mechanism behind the observed changes in IFN-gamma R expression.

Main Methods:

  • Co-culture of human PBMCs with T. cruzi.
  • Flow cytometry analysis to quantify IFN-gamma R expression on B cells (CD19+, CD20+) and T cells (CD3+).

Related Experiment Videos

  • Assessment of other B cell markers (CD19, CD20, DR) and intracellular IFN-gamma R levels.

    • Main Results:

    • T. cruzi significantly decreased IFN-gamma R expression on B cells, with effects seen as early as 3 hours and lasting up to 24 hours.
    • The parasite did not affect the expression of CD19, CD20, or DR antigens on B cells.
    • Cell-free T. cruzi filtrates mimicked the suppressive effect, and reduced intracellular IFN-gamma R levels suggested suppressed synthesis.
    • T. cruzi also reduced IFN-gamma R expression on a subset of T cells.

    Conclusions:

    • T. cruzi actively suppresses IFN-gamma R expression on human B lymphocytes, likely by inhibiting receptor synthesis.
    • This suppression of IFN-gamma R on B cells may contribute to immune evasion by T. cruzi.
    • The findings highlight a novel mechanism of immune modulation by T. cruzi impacting cellular signaling pathways.