Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
Dynamics and functional heterogeneity of FOXP3+ regulatory T cells in Trypanosoma cruzi infection: a systematic review.
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Cardozo Marcelo Eduardo, Cirilo Tatyane Martins, de Oliveira Ana Laura Grossi, Antunes-Porto Ana Rafaela, do Braga Amaral Luisa Vitor, da Rocha Rihs José Bryan, Dias Magalhães Luisa Mourão, Bueno Lilian Lacerda, Machado Fabiana Simão, Fujiwara Ricardo Toshio
Аннотация
BACKGROUND: The role of regulatory T cells (Tregs) in Trypanosoma cruzi infection remains unresolved, with conflicting evidence suggesting either protection from immunopathology or impairment of parasite control.
METHODS: We performed the first systematic review integrating data on Treg phenotype and function in human and experimental Chagas disease. A comprehensive search of PubMed, Embase, Scopus, and LILACS (2003-2025) identified studies assessing Tregs during T. cruzi infection. Study selection, data extraction, and risk-of-bias assessment followed PRISMA 2020 and Cochrane guidelines.
RESULTS: Twenty-seven studies met eligibility criteria (9 human, 18 murine). Human studies consistently showed that individuals with indeterminate Chagas disease harbor functionally stable Tregs enriched for CD39, CD25high, and CTLA-4 expression. In contrast, Chagas cardiomyopathy was associated with Treg instability, PD-1 upregulation, and partial acquisition of Th1-like features. Murine models revealed a phase-dependent role: transient Treg restriction during acute infection enhanced CD8⁺ T cell-mediated parasite control, whereas failure to re-establish regulatory balance promoted chronic cardiac inflammation. Key modulatory pathways included IL-10, IL-2, IL-33/ST2, G-CSF, and CD39.
CONCLUSION: These findings support a dual-role model in which Tregs dynamically coordinate disease tolerance. Treg-associated signatures, particularly CD39 expression and activated/resting Treg ratios, emerge as promising biomarkers and therapeutic targets for Chagas disease.
METHODS: We performed the first systematic review integrating data on Treg phenotype and function in human and experimental Chagas disease. A comprehensive search of PubMed, Embase, Scopus, and LILACS (2003-2025) identified studies assessing Tregs during T. cruzi infection. Study selection, data extraction, and risk-of-bias assessment followed PRISMA 2020 and Cochrane guidelines.
RESULTS: Twenty-seven studies met eligibility criteria (9 human, 18 murine). Human studies consistently showed that individuals with indeterminate Chagas disease harbor functionally stable Tregs enriched for CD39, CD25high, and CTLA-4 expression. In contrast, Chagas cardiomyopathy was associated with Treg instability, PD-1 upregulation, and partial acquisition of Th1-like features. Murine models revealed a phase-dependent role: transient Treg restriction during acute infection enhanced CD8⁺ T cell-mediated parasite control, whereas failure to re-establish regulatory balance promoted chronic cardiac inflammation. Key modulatory pathways included IL-10, IL-2, IL-33/ST2, G-CSF, and CD39.
CONCLUSION: These findings support a dual-role model in which Tregs dynamically coordinate disease tolerance. Treg-associated signatures, particularly CD39 expression and activated/resting Treg ratios, emerge as promising biomarkers and therapeutic targets for Chagas disease.