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Leishmania amazonensis infection induces PD-L1 expression on dendritic cells and impairs Th1 responses in vitro and in vivo.

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Scientific reports 📖 저널 OA 97.4% 2021: 24/24 OA 2022: 32/32 OA 2023: 45/45 OA 2024: 140/140 OA 2025: 938/938 OA 2026: 718/767 OA 2021~2026 2025 Vol.15(1) p. 37856
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de Matos Guedes HL, da Fonseca-Martins AM, Liang Y, Carlsen ED, Henard CA, Pinchuk IV

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Leishmania amazonensis is an etiological agent of diffuse cutaneous leishmaniasis in South America.

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APA de Matos Guedes HL, da Fonseca-Martins AM, et al. (2025). Leishmania amazonensis infection induces PD-L1 expression on dendritic cells and impairs Th1 responses in vitro and in vivo.. Scientific reports, 15(1), 37856. https://doi.org/10.1038/s41598-025-21669-0
MLA de Matos Guedes HL, et al.. "Leishmania amazonensis infection induces PD-L1 expression on dendritic cells and impairs Th1 responses in vitro and in vivo.." Scientific reports, vol. 15, no. 1, 2025, pp. 37856.
PMID 41162467 ↗

Abstract

Leishmania amazonensis is an etiological agent of diffuse cutaneous leishmaniasis in South America. In murine models, dysfunctional expansion of effector T cells and Th1 response exhaustion are linked to pathogenesis, while regulatory T cells (Tregs) promote lesion resolution. This study examined the roles of PD-1 and PD-L1 in the immunopathogenesis of L. amazonensis infection in C57BL/6 mice. We found a significant increase in PD-1 and PD-L1 expression in infected tissues, correlating with increased PD-L1CD11c dendritic cells (DCs) and PD-1CD4 T cells in draining lymph nodes. Infection of bone marrow-derived DCs (BMDCs) with promastigotes and amastigotes revealed that PD-L1 expression was induced by mTOR, partially by STAT3, PI3K, and MAPK. Infected BMDCs in vitro inhibited Th1 cell expansion compared to non-infected BMDCs. In vivo experiments showed that PD-L1 mice exhibited increased Th1 responses, reduced lesion sizes, and lower parasite loads. These results suggest a non-protective role for PD-1/PD-L1 signaling in regulating local immune responses during L. amazonensis infection, providing new insights into immune regulation in New World cutaneous leishmaniasis.

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