Goldstein Nathaniel B, Koster Maranke I, Hoaglin Laura G, Spoelstra Nicole S, Kechris Katerina J, Robinson Steven E, Robinson William A, Roop Dennis R, Norris David A, Birlea Stanca A
Department of Dermatology, University of Colorado Anschutz Medical Campus, School of Medicine, Aurora, Colorado, USA.
Department of Dermatology, University of Colorado Anschutz Medical Campus, School of Medicine, Aurora, Colorado, USA; Charles C. Gates Center for Regenerative Medicine and Stem Cell Biology, Department of Dermatology, University of Colorado Anschutz Medical Campus, School of Medicine, Aurora, Colorado, USA.
J Invest Dermatol. 2015 Aug;135(8):2068-2076. doi: 10.1038/jid.2015.126. Epub 2015 Mar 30.
In vitiligo, the autoimmune destruction of epidermal melanocytes produces white spots that can be repigmented by melanocyte precursors from the hair follicles, following stimulation with UV light. We examined by immunofluorescence the distribution of melanocyte markers (C-KIT, DCT, PAX3, and TYR) coupled with markers of proliferation (KI-67) and migration (MCAM) in precursors and mature melanocytes from the hair follicle and the epidermis of untreated and narrow band UVB (NBUVB)-treated human vitiligo skin. NBUVB was associated with a significant increase in the number of melanocytes in the infundibulum and with restoration of the normal melanocyte population in the epidermis, which was lacking in the untreated vitiligo. We identified several precursor populations (melanocyte stem cells, melanoblasts, and other immature phenotypes), and progressively differentiating melanocytes, some with putative migratory and/or proliferative abilities. The primary melanocyte germ was present in the untreated and treated hair follicle bulge, whereas a possible secondary melanocyte germ composed of C-KIT+ melanocytes was found in the infundibulum and interfollicular epidermis of UV-treated vitiligo. This is an exceptional model for studying the mobilization of melanocyte stem cells in human skin. Improved understanding of this process is essential for designing better treatments for vitiligo, ultimately based on melanocyte stem cell activation and mobilization.
在白癜风中，表皮黑素细胞的自身免疫性破坏会产生白斑，在紫外线照射刺激后，毛囊中的黑素细胞前体可使其重新色素沉着。我们通过免疫荧光检查了黑素细胞标志物（C-KIT、DCT、PAX3和TYR）与增殖标志物（KI-67）和迁移标志物（MCAM）在未治疗和窄谱中波紫外线（NBUVB）治疗的人类白癜风皮肤的毛囊和表皮中的前体黑素细胞和成熟黑素细胞中的分布。NBUVB与漏斗部黑素细胞数量的显著增加以及表皮中正常黑素细胞群体的恢复有关，而未治疗的白癜风表皮中缺乏这种正常黑素细胞群体。我们鉴定出了几个前体群体（黑素细胞干细胞、成黑素细胞和其他未成熟表型）以及逐渐分化的黑素细胞，其中一些具有假定的迁移和/或增殖能力。原发性黑素细胞生发部位存在于未治疗和治疗后的毛囊隆突中，而在紫外线治疗的白癜风的漏斗部和毛囊间表皮中发现了一个可能由C-KIT+黑素细胞组成的继发性黑素细胞生发部位。这是研究人类皮肤中黑素细胞干细胞动员的一个特殊模型。更好地理解这一过程对于设计更好的白癜风治疗方法至关重要，最终基于黑素细胞干细胞的激活和动员。
