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Published on: June 22, 2016
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.
Insights
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+).
- 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.
Abstract:
A substantial proportion of human peripheral blood mononuclear cells (PBMC) manifested a decreased capacity to express membrane interferon-gamma receptors (IFN-gamma R) when co-cultured with Trypanosoma cruzi. Among the lymphocytes, B cells accounted for the bulk of this effect, evidenced by a marked drop in the proportion of CD19+ or CD20+ cells expressing IFN-gamma R. Decreased IFN-gamma R expression by B lymphocytes was seen as early as 3 h after co-culture with T. cruzi and persisted for at least 24 h. The parasite had no detectable effect on CD19, CD20 or DR antigen expression by B lymphocytes. Neither the proportion of B cells expressing these markers nor the membrane density of these molecules varied significantly in the presence of T. cruzi. In PBMC cultures stimulated with Staphlyococcus aureus Cowan I (SACI), T. cruzi decreased the percentages of both IFN-gamma R+ and IFN-R+bright (cells expressing above-normal levels of surface IFN-gamma R) B lymphocytes. Cell-free filtrates of T. cruzi suspensions reproduced the suppressive effects of living parasites on IFN-gamma R expression by B cells. When T. cruzi present, the intracellular levels of IFN-gamma R molecules in resting or SACI-activated B lymphocytes, represented by fluorescence intensity, were well below control values, suggesting that decreased surface expression resulted from suppressed IFN-gamma R synthesis. Among T (CD3+) cells, 10.8% to 39.6% (7 donors) expressed surface IFN-gamma R and did so at a very low level. These percentages were also reduced by T. cruzi.(ABSTRACT TRUNCATED AT 250 WORDS)
