PMC:5767236 / 20819-21943 JSONTXT

{"target":"http://pubannotation.org/docs/sourcedb/PMC/sourceid/5767236","sourcedb":"PMC","sourceid":"5767236","source_url":"https://www.ncbi.nlm.nih.gov/pmc/5767236","text":"Figure 3 Role of macrophages in the immune response against Trypanosoma cruzi infection. Macrophages are the main infiltrating cells arriving to the myocardium early after T. cruzi infection. Different mediators can regulate the magnitude and quality of the cardiac immune response by modulating macrophages activation. (A) ATP is released by infected/injured cells and hydrolyzed by two ectoenzymes, CD39 and CD73, to the immunoregulatory metabolite ADO. Pharmacological inhibition of CD73 activity with APCP enhances M1 over M2 macrophage phenotype and increases the local production of TNF, IL-1β, IL-6, and NO and diminished IL-10 levels. (B) IL-6 is a pleiotropic cytokine that contributes to the establishment of cardiac M2 macrophage profile during T. cruzi infection by inducing an anti-inflammatory microenvironment and augmented CD39 expression. Deficiency of IL-6 (IL6KO mice) dysregulates inflammasome activation with a consequent increases in IL1-β-induced NO production. The excessive oxidative stress and exacerbated pro-inflammatory immune response cause the lethal effect observed in infected IL6KO mice. ","tracks":[]}