ArticleThe American journal of pathology2007
Fas ligand-dependent inflammatory regulation in acute myocarditis induced by Trypanosoma cruzi infection.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 45 citations in OpenAlex.
- The Liver and the Hepatic Immune Response inPathogens (Basel, Switzerland) · 2021Review
- Physical Exercise Promotes a Reduction in Cardiac Fibrosis in the Chronic Indeterminate Form of Experimental Chagas Disease.Frontiers in immunology · 2021Article
- Multiparametric Color Tendency Analysis (MCTA): A Method to Analyze Several Flow Cytometry Labelings Simultaneously.Frontiers in bioengineering and biotechnology · 2020Article
- CD43 sialoglycoprotein modulates cardiac inflammation and murine susceptibility to Trypanosoma cruzi infection.Scientific reports · 2019Article
- Reverse Signaling of Tumor Necrosis Factor Superfamily Proteins in Macrophages and Microglia: Superfamily Portrait in the Neuroimmune Interface.Frontiers in immunology · 2019Review
- HMGB1 release triggered by the interaction of live retinal cells and uveitogenic T cells is Fas/FasL activation-dependent.Journal of neuroinflammation · 2015Article
- Increase in the expression of CD4 + CD25+ lymphocytic T cells in the indeterminate clinical form of human Chagas disease after stimulation with recombinant antigens of Trypanosoma cruzi.Journal of clinical immunology · 2014Article
- Moderate physical exercise protects myenteric metabolically more active neurons in mice infected with Trypanosoma cruzi.Digestive diseases and sciences · 2014Article
- Moderate physical exercise reduces parasitaemia and protects colonic myenteric neurons in mice infected with Trypanosoma cruzi.International journal of experimental pathology · 2013Article
- Mast cell function and death in Trypanosoma cruzi infection.The American journal of pathology · 2011Article
- Apoptosis induced by parasitic diseases.Parasites & vectors · 2010Article
- Fas (CD95) induces rapid, TLR4/IRAK4-dependent release of pro-inflammatory HMGB1 from macrophages.Journal of inflammation (London, England) · 2010Article
- Acute Trypanosoma cruzi experimental infection induced renal ischemic/reperfusion lesion in mice.Parasitology research · 2009Article
- Alterations in myocardial gene expression associated with experimental Trypanosoma cruzi infection.Genomics · 2008Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fas/Fas ligand (Fas-L) engagement, a potent inducer of apoptosis, is also important for cellular activation, regulation of effector and chemotactic activity, and secretion of chemokines and cytokines. We evaluated the relevance of Fas/Fas-L in the regulation of myocarditis induced by Trypanosoma cruzi infection and observed that in Fas-L(-/-) mice (gld/gld), cardiac infiltration was significantly reduced, accordingly showing less cardiomyocyte destruction. Fluorescence-activated cell sorting analysis of cardiac inflammatory cells showed higher numbers of CD8(+) T cells in BALB/c compared with gld/gld mice but similar levels of lymphocyte function-associated antigen-1, intercellular adhesion molecule, CD2, and CD69 expression; MAC-1(+) myeloid cells and mast cells were increased in BALB/c mice, whereas gld/gld mice exhibited an enrichment of CD4(+/low) T cells. Intracellular labeling of cytokines revealed no clear cardiac skewing of Th1 or Th2 responses, but we found a higher number of interleukin-10(+) cells in gld/gld mice and a deficient expression of vascular cell adhesion molecule-1 on cardiac endothelial cells in gld/gld mice. Finally, we found a population of CD3(+) but CD4/CD8 double negative cardiac T cells in both groups of infected mice, but down-regulation of some adhesion molecules and surface receptors was only observed in gld/gld mice, indicating a targeted T-cell population mostly affected by the lack of Fas-L engagement. These results point to a role for myocarditis regulation by Fas/Fas-L beyond its possible direct relevance in cellular death.
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