特应性皮炎肿瘤坏死因子相关凋亡诱导配体(TRAIL)表达增强和潜在的抗炎作用

作     者：Vassina E. LeverkusM. Yousefi S. D. Simon 任建文 

作者机构：Department of Dermatology Inselspital University of Bern CH- 3010 Bern Switzerland Dr. 

出 版 物：《世界核心医学期刊文摘（皮肤病学分册）》 (Digest of the World Core Medical JOurnals:Dermatology)

年 卷 期：2006年第2卷第8期

页      面：15-15页

学科分类：1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100101[医学-人体解剖与组织胚胎学] 100206[医学-皮肤病与性病学] 10[医学] 

主　　题：肿瘤坏死因子相关凋亡诱导配体 特应性皮炎 IL-1受体拮抗剂 抗炎作用 表达增强 表皮角质形成细胞 TRAIL受体 外周血T细胞 AD患者 潜在 

摘      要：The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis of many transformed but also of non-transformed cells. In addition, TRAIL receptor activation has been reported to activate non-apoptotic signaling pathways. Here, we report an increased expression of TRAIL in peripheral blood T cells and monocytes from patients with atopic dermatitis (AD) compared with control individuals. High TRAIL expression was also observed in skin-infiltrating T cells of AD patients. Topical tacrolimus treatment reduced the total number of T cells in the skin, but the relative proportion of TRAIL-positive cells within both CD4+ and CD8+ cell populations did not change. TRAIL was demonstrated to induce the expression of interleukin-1 receptor antagonist (IL-1Ra) in keratinocytes in a caspase-independent manner in vitro. Moreover, increased expression of IL-1Ra was observed in keratinocytes of Ad lesional skin. These data suggest that TRAIL-expressing inflammatory skin cells may contribute to the epidermal activation of the IL-1Ra gene in AD.