Immune dysregulation and inflammation causing hypopigmentation in post kala-azar dermal leishmaniasis: partners in crime?

Autor: Sengupta R; Dept. of Pharmacology, Institute of Post Graduate Medical Education and Research, 244B AJC Bose Road, Kolkata 700020, India., Roy M; Dept. of Pharmacology, Institute of Post Graduate Medical Education and Research, 244B AJC Bose Road, Kolkata 700020, India., Dey NS; York Biomedical Research Institute, Hull York Medical School, University of York, Heslington, York, YO10 5DD, UK., Kaye PM; York Biomedical Research Institute, Hull York Medical School, University of York, Heslington, York, YO10 5DD, UK., Chatterjee M; Dept. of Pharmacology, Institute of Post Graduate Medical Education and Research, 244B AJC Bose Road, Kolkata 700020, India. Electronic address: ilatimc@gmail.com.
Jazyk: angličtina
Zdroj: Trends in parasitology [Trends Parasitol] 2023 Oct; Vol. 39 (10), pp. 822-836. Date of Electronic Publication: 2023 Aug 15.
DOI: 10.1016/j.pt.2023.07.005
Abstrakt: Post kala-azar dermal leishmaniasis (PKDL), a heterogeneous dermal sequela of visceral leishmaniasis (VL), is challenging in terms of its etiopathogenesis. Hypopigmentation is a consistent clinical feature in PKDL, but mechanisms contributing to the loss of melanocytes remains poorly defined. Like other hypopigmentary dermatoses - for example, vitiligo, psoriasis, and leprosy - the destruction of melanocytes is likely a multifactorial phenomenon, key players being immune dysregulation and inflammation. This review focuses on immunological mechanisms responsible for the 'murder' of melanocytes, prime suspects at the lesional sites being CD8 + T cells and keratinocytes and their criminal tools being proinflammatory cytokines, for example, IFN-γ, IL-6, and TNF-α. Collectively, these may cause decreased secretion of melanocyte growth factors, loss/attenuation of cell adhesion molecules and inflammasome activation, culminating in melanocyte death.
Competing Interests: Declaration of interests The authors declare no competing interests.
(Copyright © 2023. Published by Elsevier Ltd.)
Databáze: MEDLINE
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