RESEARCH ARTICLE
Immunohistochemical Findings in Active Vitiligo Including Depigmenting Lesions and Non-Lesional Skin
Flavia M.N.P. Aslanian*, 1, Rosangela A.M. Noé1, Daniela P. Antelo1, Rogerio E. Farias2, Pranab K. Das3, Ibrahim Galadari4, Tullia Cuzzi1, Absalom L. Filgueira1
Article Information
Identifiers and Pagination:
Year: 2008Volume: 2
First Page: 105
Last Page: 110
Publisher ID: TODJ-2-105
DOI: 10.2174/1874372200802010105
Article History:
Received Date: 23/10/2008Revision Received Date: 21/11/2008
Acceptance Date: 01/12/2008
Electronic publication date: 24/12/2008
Collection year: 2008
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Background:
The evidence that vitiligo is an autoimmune disease is supported by its association with autoimmune conditions, the presence of activated cytotoxic T lymphocytes in the lesions and melanocyte-specific circulating auto-antibodies. Some studies have indicated the normal-appearing skin being immune-targeted for latent melanocyte disappearance.
Method:
We aimed to characterize immunohistologically the cellular infiltrate and to identify the distribution pattern of T and Langerhans cells (LCs) in the active border of depigmenting lesions and clinically normal skin of 22 patients with progressive non-segmental vitiligo, besides the cellular expression for the cutaneous lymphocyte-associated antigen (CLA), comparing to 10 controls.
Results:
Immunohistochemical analyses showed an overall reduction of the number of CD1a+ cells, dermal increase of CD8+ T cells, and increase of the epidermal CD3+ T cells number in the active border of lesions. Surprisingly, those cellular changes were also observed in clinically pigmented skin. However, a significant intra-epidermal infiltration of CD8+ T cells was evident only within active border biopsies. The CLA+ cells were not significantly increased in the patients’ skin.
Conclusions:
The findings of this study suggest an extensively immune-committed skin in active vitiligo, mainly characterized by overall scarcity of CD1a+ cells and dermal increase of CD8+ cells even in apparently normal skin, in addition to the epidermal infiltrate of CD8+ T cells in the depigmenting areas. This report further supports that some CD8+ T and LCs cells play a pivotal role in the process of melanocyte loss, and strengthens an auto-immune hypothesis for vitiligo.
