Trypanosoma cruzi: exposure of murine cells to live parasites in vitro leads to enhanced surface class I MHC expression which is type I interferon-dependent.

Previous reports indicate that myocardial cells from human patients with chronic Chagasic cardiomyopathy express increased levels of class I MHC molecules on their surfaces. To determine whether parasites can modulate class I expression, we have examined the effect of in vitro exposure to live Trypanosoma cruzi trypomastigotes on class I MHC expression by murine cells. Here we show that co-incubation of various murine cell lines, including 3T3 fibroblasts, J774.A1 macrophage-like cells, and freshly-explanted BALB/c primary embryo fibroblasts, with live trypomastigotes leads to a two- to fourfold increase in their expression of surface class I MHC molecules. Cell-free supernatants from T. cruzi-exposed cells, but not from either cells or parasites cultured alone, were also capable of upregulating class I expression, indicating the involvement of a soluble factor. Active supernatants were shown to contain IFN-alpha/beta activity and their ability to upregulate class I was inhibitable by anti-IFN-alpha/beta Abs. This ability of T. cruzi to enhance class I MHC expression on host cells via IFN-alpha/beta induction could be an important factor in the initiation of host immunity and/or immune-mediated pathology.