PDF(Pubmed)
Abstract：
Both alopecia areata (AA) and vitiligo are distinct, heterogenous, and complex disease entities, characterized by nonscarring scalp terminal hair loss and skin pigment loss, respectively. In AA, inflammatory cell infiltrates are in the deep reticular dermis close to the hair bulb (swarm of bees), whereas in vitiligo the inflammatory infiltrates are in the epidermis and papillary dermis. Immune privilege collapse has been extensively investigated in AA pathogenesis, including the suppression of immunomodulatory factors (e.g., transforming growth factor-β (TGF-β), programmed death-ligand 1 (PDL1), interleukin-10 (IL-10), α-melanocyte-stimulating hormone (α-MSH), and macrophage migration inhibitory factor (MIF)) and enhanced expression of the major histocompatibility complex (MHC) throughout hair follicles. However, immune privilege collapse in vitiligo remains less explored. Both AA and vitiligo are autoimmune diseases that share commonalities in pathogenesis, including the involvement of plasmacytoid dendritic cells (and interferon-α (IFN- α) signaling pathways) and cytotoxic CD8+ T lymphocytes (and activated IFN-γ signaling pathways). Blood chemokine C-X-C motif ligand 9 (CXCL9) and CXCL10 are elevated in both diseases. Common factors that contribute to AA and vitiligo include oxidative stress, autophagy, type 2 cytokines, and the Wnt/β-catenin pathway (e.g., dickkopf 1 (DKK1)). Here, we summarize the commonalities and differences between AA and vitiligo, focusing on their pathogenesis.
摘要：
斑秃（AA）和白癜风是不同的，异质，和复杂的疾病实体，其特点是无疤痕的头皮终端脱发和皮肤色素损失，分别。在AA，炎症细胞浸润在靠近毛球（蜂群）的深层网状真皮中，而在白癜风中，炎性浸润在表皮和乳头状真皮中。免疫特权崩溃在AA发病机制中已被广泛研究，包括抑制免疫调节因子(例如，转化生长因子-β（TGF-β），程序性死亡配体1（PDL1），白细胞介素-10（IL-10），α-黑素细胞刺激素(α-MSH),和巨噬细胞迁移抑制因子（MIF）），并增强了整个毛囊中主要组织相容性复合物（MHC）的表达。然而,免疫特权崩溃在白癜风中的探索仍然较少。AA和白癜风都是自身免疫性疾病，在发病机制上有共同之处。包括浆细胞样树突状细胞（和干扰素-α（IFN-α）信号通路）和细胞毒性CD8+T淋巴细胞（和激活的IFN-γ信号通路）的参与。血液趋化因子C-X-C基序配体9(CXCL9)和CXCL10在两种疾病中均升高。导致AA和白癜风的常见因素包括氧化应激，自噬,2型细胞因子，和Wnt/β-catenin途径(例如，dickkopf1(DKK1))。这里,我们总结了AA和白癜风之间的共同点和区别，专注于他们的发病机制。
