Key result
T-cell IL-18R/MyD88 signaling drives cytotoxic CD4+ T cell expansion in Trypanosoma cruzi-infected hearts.
Why the study?
The impact of cytotoxic CD4+ T cells and the mechanisms controlling their generation during Trypanosoma cruzi infection remain poorly understood.
Population
Mice infected with Trypanosoma cruzi and human Chagas patients
Comparison
WT vs Myd88-/- and Il18ra-/- mice/cells
Design
Preclinical study with knockout models and adoptive transfer experiments
Authors
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CD4CTLs merit study in Chagas disease; leaves open their role and therapeutic targeting in humans.
CD4CTLs driven by IL-18R/MyD88 signaling are major players in immunity against Trypanosoma cruzi and their frequency correlates with Chagas cardiomyopathy severity.
Barbosa et al. (2021) studied Trypanosoma cruzi infection / Chagas disease. T-cell intrinsic IL-18R/MyD88 signaling deficiency vs. Wild-type controls was evaluated on CD4+ T cell cytotoxicity and absolute numbers of CD4CTLs. T-cell intrinsic IL-18R/MyD88 signaling is critical for the expansion and survival of cytotoxic CD4+ T cells, which predominantly infiltrate Trypanosoma cruzi-infected hearts.
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