Chagas disease
Host Response and InflammationT-Cell Immunophenotyping and Cytokine Production Analysis in Patients with Chagas Disease 4 Years after Benznidazole TreatmentThe major problem with Chagas disease is evolution of the chronic indeterminate form to a progressive cardiac disease. Treatment diminishes parasitemia but not clinical progression, and the immunological features involved are unclear. Here, we studied the clinical course and the immune response in patients with chronic-phase Chagas disease at 48 months after benznidazole treatment.
Host Response and InflammationLow-Level Parasite Persistence Drives Vasculitis and Myositis in Skeletal Muscle of Mice Chronically Infected with Trypanosoma cruziIn chronic Trypanosoma cruzi infection, the cause of Chagas disease, life-threatening inflammatory diseases develop over time in the heart, esophagus, and colon of some patients. C57BL/6 mice infected with the myotropic Colombiana strain of T. cruzi model many of the immunological and...
- Cellular Microbiology: Pathogen-Host Cell Molecular InteractionsTrypanosoma cruzi Produces the Specialized Proresolving Mediators Resolvin D1, Resolvin D5, and Resolvin E2
- Microbial Immunity and VaccinesVaccine-Linked Chemotherapy Improves Benznidazole Efficacy for Acute Chagas Disease
- Fungal and Parasitic InfectionsGenetic Adjuvantation of a Cell-Based Therapeutic Vaccine for Amelioration of Chagasic Cardiomyopathy
- Fungal and Parasitic InfectionsGeneration of Trypanosoma cruzi-Specific CD8+ T-Cell Immunity Is Unaffected by the Absence of Type I Interferon Signaling
- Fungal and Parasitic InfectionsPreferential Brain Homing following Intranasal Administration of Trypanosoma cruzi