Pozdnyakova Olga, Mahalingam Meera
Department of Pathology, UMASS Medical School, Worcester, MA, USA.
J Cutan Pathol. 2008 Oct;35(10):922-5. doi: 10.1111/j.1600-0560.2007.00937.x. Epub 2008 Jun 5.
While the pathogenesis of most scarring alopecias is poorly understood, one recent study indicates destruction of follicular stem cells as a possible mechanism in lichen planopilaris, the prototypic scarring alopecia. The aim of this cross-sectional study was to ascertain the target of inflammation and to more precisely characterize the inflammatory infiltrate in various stages of primary scarring alopecias. Immunohistochemical studies were performed using a panel of antibodies that included anti-cytokeratin 15, an antibody that specifically targets follicular bulge stem cells and CD4, CD8, CD1a and human leukocyte antigen-DR to characterize the inflammatory infiltrate. Our data showing absence of follicular bulge stem cells in cases with moderate to heavy inflammation suggest involvement of the bulge region in 'early' active stages of primary scarring alopecia. The paucity of CD8+ T cells in the inflammatory infiltrate in the majority of these cases argues against a cell-mediated cytotoxic destruction of follicular bulge stem cells. Preservation of CK15+ cells in 'late' fibrotic stages of primary scarring alopecia further supports this and implies that the irreversible loss of hair follicles, the sine qua non of primary scarring alopecia, is not necessarily a consequence of T cell-mediated destruction of follicular bulge stem cells.
虽然大多数瘢痕性脱发的发病机制尚不清楚，但最近的一项研究表明，毛囊干细胞的破坏可能是扁平苔藓样毛发角化病（典型的瘢痕性脱发）的发病机制之一。这项横断面研究的目的是确定炎症靶点，并更精确地描述原发性瘢痕性脱发不同阶段的炎症浸润情况。使用一组抗体进行免疫组织化学研究，这些抗体包括抗细胞角蛋白15（一种特异性靶向毛囊隆突干细胞的抗体）以及CD4、CD8、CD1a和人类白细胞抗原-DR，以描述炎症浸润情况。我们的数据显示，在中度至重度炎症的病例中不存在毛囊隆突干细胞，这表明隆突区域参与了原发性瘢痕性脱发的“早期”活跃阶段。在大多数这些病例中，炎症浸润中CD8 + T细胞数量稀少，这与细胞介导的毛囊隆突干细胞细胞毒性破坏不符。原发性瘢痕性脱发“晚期”纤维化阶段CK15 +细胞的保留进一步支持了这一点，并表明毛囊的不可逆丧失（原发性瘢痕性脱发的必要条件）不一定是T细胞介导的毛囊隆突干细胞破坏的结果。
