# Immunoregulation of cellular immunity and tissue homeostasis during Chagas' disease

> **NIH AI R01** · NATIONAL RESEARCH COUNCIL OF ARGENTINA · 2026 · $133,400

## Abstract

PROJECT SUMMARY/ABSTRACT
Chagas disease, caused by the protozoan Trypanosoma cruzi, is endemic in Latin America but cases are
increasing in non-endemic countries, becoming a global concern. It affects 6 million people and imposes a
major economic burden due to early mortality and physical disabilities. Disease progression, from symptomless
to severe, is linked to parasite heterogeneity and a variable host immune response. Development of robust
CD8+ T cell immunity is a key element of host resistance and T. cruzi persistence and chronic Chagas disease
has been associated to suboptimal CD8+ T cell responses. Despite this, the knowledge about pathways that
promote robust protective CD8+ T cell immunity to T. cruzi remains incomplete and for instance, the metabolic
hurdles faced by effector CD8+ T cells for expansion and differentiation have been barely explored. Also, the
progression of T. cruzi infection is thought to be significantly modulated by regulatory immune responses that
limit parasite-specific immunity as well as infection-associated immunopathology by mechanisms poorly
understood. In this context, defining how effector and regulatory pathways intertwined to allow the generation
of optimal cellular immunity against T. cruzi preserving of tissue homeostasis is crucial to understand Chagas
disease pathogenesis. In this direction, our published data showed that Treg cells became activated during T.
cruzi infection and acquired phenotypic attributes that markedly changed along the infection. Thus, Treg cells
acquired features linked to the regulation of type 1 responses and limited CD8+ T cell immunity during the
infection acute phase, likely delaying parasite control and favoring chronicity. In contrast, preliminary data
demonstrate that Treg cells with tissue repair ties, which were disfavored during the acute phase, accumulated
during the chronic phase in nonlymphoid tissues considered targets of T. cruzi and reduced tissue damage.
Altogether, our findings hi

## Key facts

- **NIH application ID:** 11319791
- **Project number:** 5R01AI169482-05
- **Recipient organization:** NATIONAL RESEARCH COUNCIL OF ARGENTINA
- **Principal Investigator:** Eva V Acosta Rodriguez
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** AI
- **Fiscal year:** 2026
- **Award amount:** $133,400
- **Award type:** 5
- **Project period:** 2022-04-01T00:00:00 → 2027-03-31T00:00:00

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11319791

## Citation

> US National Institutes of Health, RePORTER application 11319791, Immunoregulation of cellular immunity and tissue homeostasis during Chagas' disease (5R01AI169482-05). Retrieved via AI Analytics 2026-07-09 from https://api.ai-analytics.org/grant/nih/11319791. Licensed CC0.

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