ArticlePLoS neglected tropical diseases2026
Role of chemokines and their receptors in lesional CD8⁺ T cell homing in Indian Post-Kala-Azar Dermal Leishmaniasis.
Article in PLoS neglected tropical diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPost-kala-azar dermal leishmaniasis (PKDL), a dermal sequel of visceral leishmaniasis (VL) is considered as a reservoir that facilitates the transmission of VL. Although PKDL lesions demonstrate an overwhelming infiltration of CD8 ⁺ T cells, characterization of lesional CD8 ⁺ T cells, their tissue-homing chemokine receptors and corresponding ligands remains poorly defined, and was the aim of this study. METHODOLOGY: In patients with PKDL, CD8 ⁺ T cells were phenotyped in skin biopsies, in terms of senescence (CD8 ⁺ /CD57⁺), and cytotoxicity (expression of Perforin and Granzyme). The plasma levels of T cell chemoattractants (CCL3/4/5/17, CXCL9/10), and associated cytokines (IFN-γ, IL-5, TNF-α, IL-15) were assessed by a multiplex assay, while their lesional expression was evaluated by bulk RNA sequencing and immunohistochemistry. Furthermore, the expression of circulating chemokine receptors, namely CCR4 (for CCL17/22), CCR5 (for CCL3), and CXCR3 (for CXCL9/10), were assessed by flow cytometry, and at lesional sites using transcriptomic data/immunofluorescence. PRINCIPAL
findingsAs compared to healthy controls, dermal lesions from PKDL patients showed a significant increase in CD8 ⁺ T cells that demonstrated exhaustion/senescence (CD8 ⁺ /CD57⁺), as also lacked Perforin and Granzyme. In circulation and lesional tissues, T cell chemoattractants (CCL 3/4/5/17, CXCL 9/10) and pro-inflammatory cytokines (IFN-γ, IL-5, IL-15 TNF-α) along with their corresponding receptors, CCR4, CCR5 and CXCR3 were elevated.
conclusionsIn dermal lesions of PKDL, an enhanced homing of CD8 ⁺ T cells was achieved via an upregulation of T cell chemoattractants CCL3/4/5/17, CXCL9/10, and their corresponding receptors. Their exhausted/senescent phenotype and loss of cytotoxicity possibly facilitated parasite persistence, highlighting the need for host directed immunotherapeutic approaches aimed at restoring T cell potency.
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