EXPRESSION OF HLA-G BY HUMAN CARDIAC MYOCYTES IN ACUTE GIANT CELL MYOCARDITIS BUT NOT IN CHRONIC CHAGASIC MYOCARDITIS

ARGUELLO R; VIGLIANO C; CABEZA MECKERT P; LAGUENS R; LAUCELLA S

París

Congreso; 6th INTERNATIONAL CONFERENCE ON HLA-G; 2012

In order to investigate differences in the immunoregulatory mechanisms between an acute myocarditis of putative immune pathogenesis and a chronic myocarditis induced by Trypanosoma cruzi infection, (chagasic cardiopathy), we measured the expression of CD3 (T cells), CD57 (effector T cells and NKs), CD68 (macrophages),FOXP3 (Regulatory T cells), Tbet (TH1 cells), CTLA-4 (inhibitory receptor), Ki67 (active cell cycle), active Caspase-3 (apoptosis), iNOS (activated macrophages) and HLA-G in explanted hearts from eight patients with chronic chagas myocarditis, and two patients with giant cell acute myocarditis (GCM) submitted to cardiac transplantation. The expression of HLA-G and Ki67 in cardiac myocytes at the sites of contact with vast presence of activated macrophages (iNOS+), some showing with high levels of active-caspase-3, was only observed in GCM. On the contrary, Tbet and Ki67 positive T cells were observed exclusively in chagasic myocarditis, evidencing a type I immune response to the parasite. In summary, both myocarditis differed in the cellular composition of the inflammatory infiltrate and in the molecular pattern of immunoregulatory protein expression. We propose that in GCM, HLA-G induction in myocytes, as a consequence of contact with the inflammatory milieu, would induce apoptosis in the activated macrophages preventing cell damage induced by macrophage products, such as NO and cytokines.