Publication: Keratinocyte dysfunction in vitiligo
epidermis: cytokine microenvironment
and correlation to keratinocyte apoptosis
Authors
Moretti, Silvia ; Fabbri, Paolo ; Baroni, Gianna ; Berti, Samantha ; Ban, Daniele ; Berti, Emilio ; Nassini, Romina ; Lotti, Torello ; Massi, Daniela
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Vitiligo is a skin disorder characterized by
loss of functional melanocytes. Keratinocytes contribute
to melanocyte homeostasis, and keratinocyte alteration
may play a role in melanocyte dysfunction in vitiligo. In
particular, the release of melanogenic mediators and the
level of functioning keratinocytes may affect melanocyte
dysfunction in vitiligo epidermis. Keratinocyte-derived
mediators involved in pigmentation, analysed by in situ
hybridization, and epidermal apoptosis, detected by
TUNEL assay and electron microscopy, were evaluated
in lesional and perilesional skin biopsies from 15
patients with active vitiligo and in 5 control subjects.
Among the melanogenic mediators, stem cell factor
(SCF) and endothelin-1 (ET-1) mRNA were
significantly reduced in lesional as compared to
perilesional epidermis, whereas no difference was
observed in mRNA of basic fibroblastic growth factor
(bFGF) and granulocyte-monocyte colony stimulating
factor (GM-CSF). The expression of mRNA for tumor
necrosis factor (TNF)-α and interleukin-6 (IL-6), two
pro-inflammatory cytokines with an inhibitory effect on
pigmentation, was increased in the epidermis from
vitiligo biopsies, whereas their expression was
practically undetectable in the skin of control subjects.
Apoptotic keratinocytes were more abundant in lesional
vs. perilesional skin of vitiligo patients and were absent
in the epidermis of control subjects. Changes in
expression of keratinocyte-derived mediators observed
in the present study are consistent with their differential
functions in melanocyte regulation. In particular,
increased TNF-α could contribute to keratinocyte
apoptosis, which results in reduced release of
melanogenic cytokines and ultimately in melanocyte
disappearance.
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