ArticleJournal of immunology (Baltimore, Md. : 1950)2012
IL-10 limits parasite burden and protects against fatal myocarditis in a mouse model of Trypanosoma cruzi infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed, 81 citations in OpenAlex.
- Article
- Protective immunity against Chagas disease induced by a superantigen-based chimeric DNA vaccine delivered by attenuatedFrontiers in immunology · 2026Article
- Cytokine Profiles and Inflammatory Implications in Chagas Disease: Associations with Ventricular Function and Conduction Disorders.Medical sciences (Basel, Switzerland) · 2025Article
- RNA and protein immunization withFrontiers in cellular and infection microbiology · 2025Article
- Animal models for exploring Chagas disease pathogenesis and supporting drug discovery.Clinical microbiology reviews · 2024Review
- Theracurmin Modulates Cardiac Inflammation in Experimental Model ofTropical medicine and infectious disease · 2023Article
- Effectiveness of Nitazoxanide and Electrolyzed Oxiding Water in Treating Chagas Disease in a Canine Model.Pharmaceutics · 2023Article
- C57BL/6 Mice Pretreated With Alpha-Tocopherol Show a Better Outcome ofFrontiers in immunology · 2022Article
- Blockage of Galectin-Receptor Interactions Attenuates Mouse Hepatic Pathology Induced byFrontiers in immunology · 2022Article
- Characterisation of Macrophage Polarisation in Mice Infected with Ninoa Strain ofPathogens (Basel, Switzerland) · 2021Article
- Aspirin-triggered resolvin D1 reduces parasitic cardiac load by decreasing inflammation in a murine model of early chronic Chagas disease.PLoS neglected tropical diseases · 2021Article
- Management of inflammation in cardiovascular diseases.Pharmacological research · 2021Review
- Oxidative stress implications for therapeutic vaccine development against Chagas disease.Expert review of vaccines · 2021Review
- Host-parasite dynamics in Chagas disease from systemic to hyper-local scales.Parasite immunology · 2021Review
- Extracellular Vesicles: Potential Role in Remote Signaling and Inflammation inFrontiers in cell and developmental biology · 2021Review
- The Blockade of Interleukin-2 During the Acute Phase ofFrontiers in cellular and infection microbiology · 2021Article
- A novel Trypanosoma cruzi secreted antigen as a potential biomarker of Chagas disease.Scientific reports · 2020Article
- A Trypsin Inhibitor fromAntibiotics (Basel, Switzerland) · 2020Article
- T-cells producing multiple combinations of IFNγ, TNF and IL10 are associated with mild forms of dengue infection.Immunology · 2020Observational
- Complete Inactivation of Blood Borne PathogenFrontiers in medicine · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Chagas' disease is a zoonosis prevalent in Latin America that is caused by the protozoan Trypanosoma cruzi. The immunopathogenesis of cardiomyopathy, the main clinical problem in Chagas' disease, has been extensively studied but is still poorly understood. In this study, we systematically compared clinical, microbiologic, pathologic, immunologic, and molecular parameters in two mouse models with opposite susceptibility to acute myocarditis caused by the myotropic Colombiana strain of T. cruzi: C3H/HeSnJ (100% mortality, uncontrolled parasitism) and C57BL/6J (<10% mortality, controlled parasitism). T. cruzi induced differential polarization of immunoregulatory cytokine mRNA expression in the hearts of C57BL/6J versus C3H/HeSnJ mice; however, most differences were small. The difference in IL-10 expression was exceptional (C57BL/6J 8.7-fold greater than C3H/HeSnJ). Consistent with this, hearts from infected C57BL/6J mice, but not C3H/HeSnJ mice, had a high frequency of total IL-10-producing CD8(+) T cells and both CD4(+) and CD8(+) subsets of IFN-γ(+)IL-10(+) double-producing T cells. Furthermore, T. cruzi infection of IL-10(-/-) C57BL/6J mice phenocopied fatal infection in wild-type C3H/HeSnJ mice with complete loss of parasite control. Adoptive transfer experiments indicated that T cells were a source of protective IL-10. Thus, in this system, IL-10 production by T cells promotes T. cruzi control and protection from fatal acute myocarditis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.