ReviewPLoS neglected tropical diseases2011
Regulatory T cells phenotype in different clinical forms of Chagas' disease.
Review in PLoS neglected tropical diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 99 citations in OpenAlex.
- Review
- ExploringAntimicrobial agents and chemotherapy · 2026Article
- IL-33/ST2 Signaling Protects the Heart by Restraining Inflammation and Parasite Burden duringACS infectious diseases · 2026Article
- Unraveling the cytokine profile in acute Chagas disease in the Brazilian Amazon: Insights before and after treatment.PLoS neglected tropical diseases · 2026Article
- 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
- Article
- Monoclonal antibodies: From magic bullet to precision weapon.Molecular biomedicine · 2024Review
- CD39 expression by regulatory T cells participates in CD8+ T cell suppression during experimental Trypanosoma cruzi infection.PLoS pathogens · 2024Article
- Signatures of CD4Frontiers in immunology · 2024Article
- Inflammation and mitochondria in the pathogenesis of chronic Chagas disease cardiomyopathy.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Association between altered tryptophan metabolism, plasma aryl hydrocarbon receptor agonists, and inflammatory Chagas disease.Frontiers in immunology · 2023Article
- Chagasic cardiomyopathy is marked by a unique signature of activated CD4Journal of translational medicine · 2022Article
- Genome-wide association study for Chagas Cardiomyopathy identify a new risk locus on chromosome 18 associated with an immune-related protein and transcriptional signature.PLoS neglected tropical diseases · 2022Article
- Revisiting the Mechanisms of Immune Evasion Employed by Human Parasites.Frontiers in cellular and infection microbiology · 2021Review
- Interleukin-9 in Immunopathology ofFrontiers in cellular and infection microbiology · 2021Article
- Monoclonal Antibodies for Protozoan Infections: A Future Reality or a Utopic Idea?Frontiers in medicine · 2021Review
- The Thymus in Chagas Disease: Molecular Interactions Involved in Abnormal T-Cell Migration and Differentiation.Frontiers in immunology · 2020Review
- Understanding CD8Trends in parasitology · 2019Review
- Role of Aryl Hydrocarbon Receptor (AhR) in the Regulation of Immunity and Immunopathology DuringFrontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD25(High) CD4+ regulatory T cells (Treg cells) have been described as key players in immune regulation, preventing infection-induced immune pathology and limiting collateral tissue damage caused by vigorous anti-parasite immune response. In this review, we summarize data obtained by the investigation of Treg cells in different clinical forms of Chagas' disease. Ex vivo immunophenotyping of whole blood, as well as after stimulation with Trypanosoma cruzi antigens, demonstrated that individuals in the indeterminate (IND) clinical form of the disease have a higher frequency of Treg cells, suggesting that an expansion of those cells could be beneficial, possibly by limiting strong cytotoxic activity and tissue damage. Additional analysis demonstrated an activated status of Treg cells based on low expression of CD62L and high expression of CD40L, CD69, and CD54 by cells from all chagasic patients after T. cruzi antigenic stimulation. Moreover, there was an increase in the frequency of the population of Foxp3+ CD25(High)CD4+ cells that was also IL-10+ in the IND group, whereas in the cardiac (CARD) group, there was an increase in the percentage of Foxp3+ CD25(High) CD4+ cells that expressed CTLA-4. These data suggest that IL-10 produced by Treg cells is effective in controlling disease development in IND patients. However, in CARD patients, the same regulatory mechanism, mediated by IL-10 and CTLA-4 expression is unlikely to be sufficient to control the progression of the disease. These data suggest that Treg cells may play an important role in controlling the immune response in Chagas' disease and the balance between regulatory and effector T cells may be important for the progression and development of the disease. Additional detailed analysis of the mechanisms on how these cells are activated and exert their function will certainly give insights for the rational design of procedure to achieve the appropriate balance between protection and pathology during parasite infections.
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