Trypanosoma cruz/‐induced decrease in the level of interferon‐7 receptor expression by resting and activated human blood lymphocytes

Abstract

A substantial proportion of human peripheral blood mononuclear cells (PBMC) manifested a decreased capacity to express membrane interferon‐γ receptors (IFN‐γR) 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‐γR. Decreased IFN‐γR 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 ofB 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‐γR+ and IFN‐R +^bnght (cells expressing above‐normal levels of surface IFN‐γR) B lymphocytes. Cell‐free filtrates of T. cruzi suspensions reproduced the suppressive effects of living parasites on IFN‐γR expression by B cells. When T. cruzi was present, the intracellular levels of IFN‐γR 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‐γR synthesis. Among T (CD3+) cells, 10–8% to 39–6% (7 donors) expressed surface IFN‐γR and did so at a very low level. These percentages were also reduced by T. cruzi. If occurring in the host, downregulated expression of IFN‐γR could curtail the utilization of IFN‐γ, known to play a critical role in host defence against T. cruzi infection.