Yamaguchi Hiroki L, Yamaguchi Yuji, Peeva Elena
Inflammation & Immunology Research Unit, Pfizer, Cambridge, MA 02139, USA.
Inflammation & Immunology Research Unit, Pfizer, Collegeville, PA 19426, USA.
Int J Mol Sci. 2024 Apr 17;25(8):4409. doi: 10.3390/ijms25084409.
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.
斑秃(AA)和白癜风都是独特的、异质性的复杂疾病实体,分别以非瘢痕性头皮终毛脱发和皮肤色素脱失为特征。在斑秃中,炎症细胞浸润位于靠近毛囊球部的深部网状真皮层(蜂群状),而在白癜风中,炎症浸润位于表皮和乳头真皮层。免疫赦免崩溃在斑秃发病机制中已得到广泛研究,包括免疫调节因子(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))的抑制以及整个毛囊中主要组织相容性复合体(MHC)表达的增强。然而,白癜风中的免疫赦免崩溃仍较少被探索。斑秃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(以及干扰素-α(IFN-α)信号通路)和细胞毒性CD8 + T淋巴细胞(以及活化的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在这两种疾病中均升高。导致斑秃和白癜风的共同因素包括氧化应激、自噬、2型细胞因子和Wnt/β-连环蛋白通路(如Dickkopf 1(DKK1))。在此,我们总结斑秃和白癜风之间的异同,重点关注它们的发病机制。