Li Mengmeng, Chen Tao, Guo Zaipei, Li Jingyi, Cao Na
Department of Dermatovenereology, West China Hospital of Sichuan University, Chengdu, China.
J Dermatol. 2013 Nov;40(11):891-5. doi: 10.1111/1346-8138.12251. Epub 2013 Aug 23.
Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK), a member of the TNF family, has been implicated as a pro-inflammatory cytokine in many types of autoimmune and infectious diseases. However, information about TWEAK in dermatological diseases is limited. To date, no studies have investigated the roles of TWEAK in patients with urticarial vasculitis (UV). This study aimed to assess serum TWEAK levels, together with TWEAK and fibroblast growth factor-inducible 14 (Fn14) expressions of skin lesions in patients with UV. Serum TWEAK levels in patients with UV, together with patients with cutaneous leukocytoclastic angiitis (CLA) and healthy controls were detected by enzyme-linked immunosorbent assay; TWEAK and Fn14 expressions of skin lesions were analyzed by immunohistochemistry. Results showed that TWEAK and Fn14 were abundantly expressed in the dermal vessel wall of lesional skin in patients with UV but not healthy controls. Serum TWEAK levels in the acute stage in patients with UV were significantly higher than those in the convalescent stage and healthy controls. Serum TWEAK levels were elevated significantly in patients with CLA compared with those in healthy controls. Our previous study indicated that TWEAK may be an important mediator for the development of vascular inflammation in skin. In addition, we also found that TWEAK blockade substantially reduced vascular damage and perivascular leukocyte infiltrates in lipopolysaccharide-induced cutaneous vasculitis. Our study shows that TWEAK may be associated with the pathogenesis of UV; it is therefore suggested that TWEAK may be a potential therapeutic target for UV and other types of cutaneous vasculitis.
肿瘤坏死因子（TNF）样凋亡弱诱导因子（TWEAK）是TNF家族的一员，在多种自身免疫性疾病和感染性疾病中被认为是一种促炎细胞因子。然而，关于TWEAK在皮肤病中的信息有限。迄今为止，尚无研究调查TWEAK在荨麻疹性血管炎（UV）患者中的作用。本研究旨在评估UV患者的血清TWEAK水平，以及UV患者皮肤病变中TWEAK和成纤维细胞生长因子诱导14（Fn14）的表达。采用酶联免疫吸附测定法检测UV患者、皮肤白细胞破碎性血管炎（CLA）患者及健康对照者的血清TWEAK水平；采用免疫组织化学法分析皮肤病变中TWEAK和Fn14的表达。结果显示，TWEAK和Fn14在UV患者病变皮肤的真皮血管壁中大量表达，而在健康对照者中未表达。UV患者急性期的血清TWEAK水平显著高于恢复期患者和健康对照者。与健康对照者相比，CLA患者的血清TWEAK水平显著升高。我们之前的研究表明，TWEAK可能是皮肤血管炎症发展的重要介质。此外，我们还发现，TWEAK阻断可显著减轻脂多糖诱导的皮肤血管炎中的血管损伤和血管周围白细胞浸润。我们的研究表明，TWEAK可能与UV的发病机制有关；因此，提示TWEAK可能是UV和其他类型皮肤血管炎的潜在治疗靶点。
