Werth Victoria P
The University of Pennsylvania and the Philadelphia Veterans Administration Hospital, Department of Dermatology 19104, USA.
Bull NYU Hosp Jt Dis. 2007;65(3):200-4.
Skin disease is the second most common manifestation in SLE patients, and a large number of patients have predominantly cutaneous lupus erythematosus. Experimental animal models suggest that modulation of immunologic factors can have a differential impact on the skin relative to the kidney, and therapeutic responses also suggest potential differences in the immunomodulation of skin relative to other organs affected in lupus. There have been recent insights into the etiology of cutaneous LE, including genetic and environmental factors. The growing understanding of the inflammatory cascade includes the role of UV-induction of pro-inflammatory cytokines, chemokines, and adhesion molecules. Apoptosis, necrosis, autoantibodies, plasmacytoid dendritic cells, T cells, B cells, and vascular changes all play a complex interactive role in the process of induction and maintenance of the lesions of cutaneous LE. Scientific efforts are beginning to clarify the pathophysiologic differences between subsets of cutaneous LE, but there are clearly many areas of investigation needed to elucidate the complex mechanisms that culminate in cutaneous LE.
皮肤疾病是系统性红斑狼疮(SLE)患者第二常见的表现,大量患者以皮肤型红斑狼疮为主。实验动物模型表明,免疫因子的调节对皮肤的影响可能与肾脏不同,治疗反应也表明皮肤免疫调节与狼疮累及的其他器官可能存在潜在差异。最近对皮肤型红斑狼疮的病因有了新的认识,包括遗传和环境因素。对炎症级联反应的深入了解包括紫外线诱导促炎细胞因子、趋化因子和黏附分子的作用。细胞凋亡、坏死、自身抗体、浆细胞样树突状细胞、T细胞、B细胞和血管变化在皮肤型红斑狼疮病变的诱导和维持过程中都发挥着复杂的相互作用。科学研究正在开始阐明皮肤型红斑狼疮各亚型之间的病理生理差异,但显然仍有许多研究领域需要探索,以阐明导致皮肤型红斑狼疮的复杂机制。