The up-regulation of HLA antigens is important during heart inflammatory events and myofibroblasts may modulate the expression of this molecule in tissues. To test this possibility, the effect of cardiac myofibroblast:macrophage contact and the production of myofibroblast inhibitor factor(s) on the macrophage HLA (Ia) expression were studied. Listeria monocytogenes-elicited Ia + peritoneal macrophages (high Ia expression) were co-cultured with cardiac myofibroblasts for 3 and 7 days (myofibroblast contact). Proteosa peptone-elicited macrophages (low Ia expression) were cultured for 3 days with interferon gamma (INF-γ) and myofibroblast conditioned medium (FCM). Ia expression was analyzed by immunofluorescence and by radioimmune assay. Myofibroblast contact induced decreased expression of Ia molecule on macrophages (p < 0.001). This was confirmed by the radioimmune analysis in macrophage: myofibroblast co-cultures (p < 0.001). Double staining for Ia and CD14 showed that only CD14 positive cells (macrophages) expressed Ia molecule. FCM was capable of diminishing Ia expression induced by INF-γ on macrophages (p < 0.001). Decreased Ia macrophage expression induced by myofibroblasts could be important in the heart inflammation's resolution, probably involving Ia redistribution on cell: cell contact and myofibroblast inhibitor factor production.
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