Specific activation of CD4- CD8- double-negative T cells by Trypanosoma cruzi-derived glycolipids induces a proinflammatory profile associated with cardiomyopathy in Chagas patients.

摘要: Summary Cardiomyopathy is the most severe outcome of Chagas disease, causing more than 12 000 deaths/year. Immune cells participate in cardiomyopathy development either by direct tissue destruction, or driving inflammation. We have shown that CD4–CD8– [double-negative (DN)] T are major sources inflammatory and anti-inflammatory cytokines, associated with cardiac (CARD) indeterminate (IND) forms respectively. Here, we sought to identify Trypanosoma cruzi-derived components lead activation DN patients. Glycolipid (GCL), lipid (LIP) protein-enriched (PRO) fractions derived from trypomastigote T. cruzi were utilized stimulate IND CARD patients determine cell evaluating CD69 cytokine expression. observed GCL, but not LIP PRO fractions, induced higher cells, especially receptor (TCR)-γδ T, CARD. GCL led an increase tumour necrosis factor (TNF) interleukin (IL)-10 expression TCR-γδ IND, while inducing IFN-γ This ratio IFN-γ/IL-10 CARD, favouring profile. These results as component responsible for chronic predominantly profile IND. findings may implications designing new strategies control prevention disease modulating response GCL.