Original Research ARTICLE
Lymphoid stress surveillance response contributes to vitiligo pathogenesis
- 1University of Tartu, Estonia
- 2Tartu University Hospital, Estonia
Vitiligo is a chronic multifactorial depigmentation disorder characterized by the destruction and functional loss of melanocytes. Although a direct cytotoxic T cell attack is thought to be responsible for melanocyte damage, the events leading to the loss of self-tolerance towards melanocytic antigens are not understood. This research aimed to identify novel cellular and molecular factors that participate in vitiligo pathogenesis. Through the application of gene expression and immunofluorescence analysis of skin biopsy samples along with immunophenotyping of circulating cells. Our study provides insights into the mechanisms involved in melanocyte destruction. The upregulation of stress-ligand MICA/MICB, recognized by activating receptors on innate and innate-like T cells, imply involvement of lymphoid stress surveillance responses in vitiligo lesions. A simultaneous increase in the expression of transcription factor EOMES that is characteristic for innate-like virtual memory T cells, suggest a similar scenario. Local lymphoid stress surveillance has been previously associated with the amplification of systemic humoral responses that were mirrored in our study by increased T follicular helper cells and switched memory B cell proportions in patients with active vitiligo. In addition, microtubule-associated protein light chain 3 staining was compatible with the activation of autophagy in keratinocytes and in the remaining melanocytes of vitiligo lesional skin.
Keywords: Vitiligo, etiology, Eomes, WIPI1, LC3, Interferons, MICA, B cells
Received: 12 Jul 2018;
Accepted: 01 Nov 2018.
Edited by:Anne Davidson, Feinstein Institute for Medical Research, United States
Reviewed by:Jillian M. Richmond, University of Massachusetts Medical School, United States
Victoria P. Werth, University of Pennsylvania, United States
Copyright: © 2018 Raam, Kaleviste, Šunina, Hermann, Saare, Prans, Pihlap, Abram, Karelson, Peterson, Rebane, Kisand and Kingo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Dr. Kai Kisand, University of Tartu, Tartu, 50090, Tartu County, Estonia, firstname.lastname@example.org
Prof. Külli Kingo, University of Tartu, Tartu, 50090, Tartu County, Estonia, email@example.com