Type 1 interferon signature in the scalp lesions of alopecia areata
Type 1 interferon signature in the scalp lesions of alopecia areata
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DOI：
10.1111/j.1365-2133.2010.09775.x
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发表时间：
2010-07-01
影响因子：
10.3
通讯作者：
Dutz, J. P.
中科院分区：
文献类型：
--
作者：
Ghoreishi, M.;Martinka, M.;Dutz, J. P.
P>背景 CD8+ T 细胞和 Th1 细胞因子对生长期毛囊球部区域的自身免疫攻击已被认为会导致斑秃 (AA) 脱发。起始刺激未知。由于α干扰素治疗可能引发AA，我们推测1型干扰素参与了疾病的诱发。目的比较AA患者的头皮病变与局部1型干扰素相关蛋白表达相关的皮肤病头皮病变。方法AA、盘状红斑狼疮、毛发扁平苔藓和雄激素性皮肤病患者的头皮病变 通过免疫组织化学检查脱发中 1 型干扰素诱导粘病毒蛋白 A (MxA)、趋化因子受体 CXCR3、细胞毒性蛋白颗粒酶 B (GrB) 和 T 细胞胞浆内抗原 1 (TiA-1) 的表达。结果 MxA 在皮内和皮下区室中表达 炎症性 AA 中毛囊（包括皮脂腺）的病变与瘢痕性脱发（盘状红斑狼疮、扁平苔藓）的病变相似，但 AA 的表皮室中不存在，非炎性 AA 或雄激素性脱发中则完全不存在。 CXCR3 表达细胞的位置与 MxA 表达相关。与疤痕性脱发相比，AA 毛囊周围的炎症细胞包括较少数量的 GrB+ 和 TiA-1+ 细胞，并且 TiA-1+ 表达占主导地位。结论我们证明 AA 炎症病变中存在 1 型干扰素相关蛋白的表达。 AA 中干扰素特征和细胞毒性相关蛋白的分布模式与疤痕性脱发不同。
P>BackgroundAutoimmune attack of the bulbar region of anagen phase hair follicles by CD8+ T cells and Th1 cytokines has been proposed to result in hair loss in alopecia areata (AA). The initiating stimuli are unknown. As interferon-alpha therapy may trigger AA, we propose that type 1 interferons are involved in the induction of disease.ObjectivesTo compare lesional scalp from patients with AA with scalp lesions of cutaneous diseases associated with local type 1 interferon-related protein expression.MethodsLesional scalp of patients with AA, discoid lupus erythematosus, lichen planopilaris and androgenetic alopecia was examined by immunohistochemistry for expression of the type 1 interferon-inducible myxovirus protein A (MxA), the chemokine receptor CXCR3, and the cytotoxic proteins granzyme B (GrB) and T-cell intracytoplasmic antigen 1 (TiA-1).ResultsMxA was expressed in the intradermal and subcutaneous compartments of the hair follicle including sebaceous glands in inflammatory AA similar to lesions of cicatricial alopecia (discoid lupus erythematosus, lichen planopilaris) but not in the epidermal compartment of AA, and not at all in noninflammatory AA or androgenetic alopecia. The location of CXCR3-expressing cells correlated with MxA expression. The inflammatory cells around the hair follicle in AA included a lower number of GrB+ and TiA-1+ cells compared with cicatricial alopecia and demonstrated predominant TiA-1+ expression.ConclusionsWe demonstrate the expression of type 1 interferon-related proteins in the inflammatory lesions of AA. The distribution pattern of the interferon signature and cytotoxicity-associated proteins in AA differs from cicatricial alopecia.