ArticlePLoS pathogens2025
Dynamics of tissue repair regulatory T cells and damage in acute Trypanosoma cruzi infection.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Review
- IL-33/ST2 Signaling Sustains Hepato-Intestinal Homeostasis by Orchestrating Vascular Surveillance and Immune Regulatory Circuits During Experimental Trypanosoma cruzi Infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Article
- Tissue-distinct Features of Follicular Cytotoxic CD8bioRxiv : the preprint server for biology · 2026Article
- IL-33/ST2 Signaling Protects the Heart by Restraining Inflammation and Parasite Burden duringACS infectious diseases · 2026Article
- Follicular CD8+ T cells in Trypanosoma cruzi infection: helpers or killers depending on the target B cell population.PLoS pathogens · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
Tissue-repair regulatory T cells (trTregs) comprise a specialized cell subset essential for tissue homeostasis and repair. While well-studied in sterile injury models, their role in infection-induced tissue damage and antimicrobial immunity is less understood. We investigated trTreg dynamics during acute Trypanosoma cruzi infection, marked by extensive tissue damage and strong CD8+ immunity. Unlike sterile injury models, trTregs significantly declined in secondary lymphoid organs and non-lymphoid target tissues during infection, correlating with systemic and local tissue damage, and downregulation of function-associated genes in skeletal muscle. This decline was linked to decreased systemic IL-33 levels, a key trTreg growth factor, and promoted by the Th1 cytokine IFN-γ. Early recombinant IL-33 treatment increased trTregs, type 2 innate lymphoid cells, and parasite-specific CD8+ cells at specific time points after infection, leading to reduced tissue damage, lower parasite burden, and improved disease outcome. Our findings not only provide novel insights into trTregs during infection but also highlight the potential of optimizing immune balance by modulating trTreg responses to promote tissue repair while maintaining effective pathogen control during infection-induced injury.
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Registered trials
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