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- W4386815545 abstract "Abstract An imbalance between suppressor and effector immune responses may preclude cure in chronic parasitic diseases. In the case of Trypanosoma cruzi infection, specialized regulatory Foxp3+ T (Treg) cells suppress protective type-1 effector responses. Herein, we investigated the kinetics and underlying mechanisms behind the regulation of protective parasite-specific CD8+ T cell immunity during acute T. cruzi infection. Using the DEREG mouse model, we found that Treg cells play a critical role during the initial stages after T. cruzi infection, subsequently influencing CD8+ T cells. Early Treg cell depletion increased the frequencies of polyfunctional short-lived, effector T cell subsets, without affecting memory precursor cell formation or the expression of activation markers. In addition, Treg cell depletion during early infection minimally affected the antigen-presenting cell response but it boosted CD4+ T cell responses before the development of anti-parasite effector CD8+ T cell responses. Crucially, the absence of CD39 expression on Treg cells significantly bolstered effector parasite-specific CD8+ T cell responses, leading to improved parasite control during T. cruzi infection. Our work underscores the crucial role of Treg cells in regulating protective anti-parasite immunity and provides evidence that CD39 expression by Treg cells represents a key immunomodulatory mechanism in this infection model." @default.
- W4386815545 created "2023-09-18" @default.
- W4386815545 creator A5002322356 @default.
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- W4386815545 date "2023-09-16" @default.
- W4386815545 modified "2023-10-14" @default.
- W4386815545 title "CD39 expression by regulatory T cells drives CD8+ T cell suppression during experimental Trypanosoma cruzi infection" @default.
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- W4386815545 doi "https://doi.org/10.1101/2023.09.14.557792" @default.
- W4386815545 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37745571" @default.
- W4386815545 hasPublicationYear "2023" @default.
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