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• W2914652563 abstract "Abstract Post Kala-azar dermal leishmaniasis (PKDL), caused by Leishmania donovani is the dermal sequel of Visceral Leishmaniasis and importantly, is the proposed disease reservoir. The survival of Leishmania parasites within monocytes/macrophages hinges on its ability to effectively nullify immune activation mechanisms. Thus, delineating the disease-promoting immune mechanisms can facilitate development of immunotherapeutic strategies. Accordingly, in the absence of an animal model, this study aimed to delineate the status of CD8 + T-cells in patients with PKDL. At disease presentation, the absence of CD4 + T-cells at lesional sites was concomitant with an overwhelming infiltration of CD8 + T-cells that demonstrated an absence of Perforin, Granzyme and Zap-70, along with an enhanced expression of Programmed Death-1 (PD-1) and the skin-homing CCL17. Additionally, the lesional CCR4 + CD8 + population was associated with an enhanced expression of IL-10 and IL-5. In circulation, the enhanced CD8 + CCR4 + T-cell population and raised levels of CCL17/22 was associated with an increased frequency of PD-1, while CD127 was decreased. Taken together, in PKDL, the enhanced plasma and lesional CCL17 accounted for the dermal homing of CD8 + CCR4 + T-cells, that along with a concomitant upregulation of PD-1 and IL-10 mediated immune inactivation, emphasizing the need for designing immunotherapies capable of reinvigorating T-cell potency." @default.
• W2914652563 created "2019-02-21" @default.
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• W2914652563 date "2019-01-24" @default.
• W2914652563 modified "2023-10-16" @default.
• W2914652563 title "Impaired activation of lesional CD8+ T-cells is associated with enhanced expression of Programmed Death-1 in Indian Post Kala-azar Dermal Leishmaniasis" @default.
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• W2914652563 doi "https://doi.org/10.1038/s41598-018-37144-y" @default.
• W2914652563 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6345993" @default.
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