bioRxivImmunologyPreprint
Th17 cells provide direct protective effects that limit stomach parasite burden following orogastric mucosal Trypanosoma cruzi infection
C. W. Cai, C. S. Eickhoff, K. A. Meza, J. R. Blase, R. E. Audette, D. H. Chan, K. A. Bockerstett, R. J. DiPaolo, D. F. Hoft
Abstract
Trypanosoma cruzi is the intracellular parasite of Chagas disease, a chronic condition characterized by cardiac and gastrointestinal morbidity. Protective immunity requires CD4+ T cells, and Th1 cells and IFN-{gamma} are important players in host defense. More recently, Th17 cells and IL-17 have been shown to exert protective functions in systemic T. cruzi infection. However, it remains unclear whether Th17 cells and IL-17A protect against mucosal infection, which is an important cause of human outbreaks. We found that IL-17RA knock-out (KO) mice are highly susceptible to orogastric infection, indicating an important function for this cytokine in mucosal immunity to T. cruzi. To investigate the specific role of Th17 cells for mucosal immunity, we reconstituted RAG1 KO mice with T. cruzi-specific T cell receptor transgenic Th17 cells prior to orogastric T. cruzi challenges. We found that Th17 cells provided protection against gastric mucosal T. cruzi infection, indicated by significantly lower stomach parasite burdens. In vitro macrophage infection assays revealed that protection by Th17 cells is reversed with IL-17A neutralization or loss of macrophage NADPH oxidase activity. Consistent with this, in vivo, mice lacking functional NADPH oxidase were not protected by Th17 cell transfer. These data are the first report that Th17 cells protect against mucosal T. cruzi infection, and identify a novel protective mechanism involving the induction of NADPH oxidase activity in macrophages by IL-17A. These studies provide important insights for Chagas vaccine development, and more broadly, increase our understanding of the diverse roles of Th17 cells in host defense.
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- IL-17RA-signaling modulates CD8+ T cell survival and exhaustion during Trypanosoma cruzi infection
J. Tosello Boari, C. L. Araujo Furlan, … E. Acosta Rodriguez·bioRxiv·May 11, 2018
- Galectin-1-deficient mice are protected against Trypanosoma cruzi infection through altered neutrophil migration and production of reactive oxygen species and nitric oxide
T. B. Riul, H. Sales-Campos, … M. D. Baruffi·bioRxiv·Sep 11, 2020
- Incomplete recruitment of protective T cells facilitates Trypanosoma cruzi persistence in the mouse colon
A. I. Ward, M. D. Lewis, … J. M. Kelly·bioRxiv·Feb 26, 2021
- CD39 expression by regulatory T cells drives CD8+ T cell suppression during experimental Trypanosoma cruzi infection
C. L. A. Furlan, S. Boccardo, … E. V. A. Rodriguez·bioRxiv·Sep 14, 2023
- Tissue damage during acute Trypanosoma cruzi infection is associated with reduced reparative regulatory T cell response and can be attenuated by early interleukin-33 administration.
Santiago Boccardo, Constanza Rodríguez, … Eva V. Acosta Rodríguez·PLoS PathogensPeer-reviewed·Jan 30, 2025
- Cytotoxic CD4+ T cells driven by T-cell intrinsic IL-18R/MyD88 signaling predominantly infiltrate Trypanosoma cruzi-infected hearts
C.-H. D. Barbosa, F. B. Canto, … M. Bellio·eLifePeer-reviewed·Jun 7, 2022