Upadhya Sathvik, Andrade Melisa J, Shukla Vaibhav, Rao Raghavendra, Satyamoorthy Kapaettu
Department of Cell and Molecular Biology, Manipal School of Life Sciences, Manipal Academy of Higher Education, Manipal, Karnataka 576104, India.
Department of Chemical Biomolecular Engineering, University of California Irvine, Irvine, CA 92697, USA.
Autoimmun Rev. 2025 Jul 31;24(8):103841. doi: 10.1016/j.autrev.2025.103841. Epub 2025 Jun 3.
Vitiligo is a hypopigmentary skin disease condition affecting local melanocytes leading to the white patched/macules of depigmented skin due to their progressive loss of melanocytes in the epidermis. Vitiligo pathogenesis involves complex interaction of several trigger factors including genetic predispositions, environmental stimuli, oxidative stress, immunological dysregulation, and impaired melanocyte function. Genetic studies have provided insight into the essential aspects related to immunological modulation, melanocyte biology and the oxidative stress response, aiding in understanding the possible mechanisms underlying vitiligo susceptibility. Epigenetic modifications further contribute to the regulatory landscape controlling the pathophysiology of this disease. While genetic studies identified key susceptibility loci, it is the functional studies that have driven the development of novel targeted therapies. Although vitiligo exhibits complex heterogenous clinical manifestations and multiple contributing factors, significant advancements have been achieved in understanding the underlying mechanism of the disease. Particularly, cytotoxic T-cell activity and interferon-gamma (IFN-ϒ) mediated immune response have been studied extensively in disease pathogenesis. This has led to the development of novel targeted therapies including cytokine targeted therapies, Janus-activated kinase (JAK) signaling inhibitors, and Wnt signaling agonists which have shown potential clinical success.
白癜风是一种色素减退性皮肤病，影响局部黑素细胞，由于表皮中黑素细胞逐渐丧失，导致皮肤出现白色斑块/斑片。白癜风的发病机制涉及多种触发因素的复杂相互作用，包括遗传易感性、环境刺激、氧化应激、免疫失调和黑素细胞功能受损。遗传学研究为与免疫调节、黑素细胞生物学和氧化应激反应相关的重要方面提供了见解，有助于理解白癜风易感性的潜在机制。表观遗传修饰进一步影响了控制该疾病病理生理学的调控格局。虽然遗传学研究确定了关键的易感基因座，但正是功能研究推动了新型靶向治疗的发展。尽管白癜风表现出复杂的异质性临床表现和多种促成因素，但在了解该疾病的潜在机制方面已取得了重大进展。特别是，细胞毒性T细胞活性和干扰素-γ（IFN-ϒ）介导的免疫反应在疾病发病机制中得到了广泛研究。这导致了新型靶向治疗的发展，包括细胞因子靶向治疗、 Janus激酶（JAK）信号抑制剂和Wnt信号激动剂，这些治疗已显示出潜在的临床成功。
