Pigmented necrobiosis lipoidica accompanied by insulin-dependent diabetes mellitus induces CD163⁺ proinflammatory macrophages and interleukin-17-producing cells.
Pigmented necrobiosis lipoidica accompanied by insulin-dependent diabetes mellitus induces CD163⁺ proinflammatory macrophages and interleukin-17-producing cells.
复制标题
色素性坏死性脂质伴随胰岛素依赖性糖尿病诱导 CD163⁺ 促炎巨噬细胞和白细胞介素 17 产生细胞。
作者：
Chihiro Wakusawa;T. Fujimura;Y. Kambayashi;S. Furudate;A. Hashimoto;S. Aiba
类脂质渐进性坏死（NL）是一种罕见的慢性肉芽肿性皮肤病，其病因不明，表现为黄褐色炎性斑块，边缘凸起，中心萎缩（1，2）。NL通常出现在前小腿，病变通常是双侧的。三分之二的此类病例发生在糖尿病患者中（2）。最近，一些报道表明，通过生物制剂（如依那西普、英夫利昔单抗）或他克莫司中和促炎细胞因子是NL的最佳治疗方法之一（1，3）。胰岛素依赖型1型糖尿病（IDDM）是一种慢性自身免疫性疾病，由选择性破坏胰腺产胰岛素B细胞引起（3）。自身免疫仅在中枢或外周耐受屏障被破坏时发生，允许自身反应性T细胞活化（4）。最近，据报道Thi 7免疫与IDDM相关（5）。我们在此描述了1例与胰岛素依赖型糖尿病相关的中性粒细胞淋巴瘤，并证实了肉芽肿形成细胞的免疫组织化学染色，特别是IL-17产生细胞和CD 163 * 促炎巨噬细胞。
Necrobiosis lipoidica (NL) is a rare chronic granulomatous skin disorder of unknown origin presenting as yellow-brown inflamrnatory plaques with raised borders and an atrophie centre (1, 2). NL typically appears on the anterior lower legs, and lesions are usually bilateral. Two-thirds of such cases are found in diabetic patients (2). Recently, several reports have suggested that neutralization of proinflammatory cytokines by biological agents (e.g. etanercept, infliximab) or tacrolimus is one ofthe optimal therapies forNL (1,3). Insulin-dependent type 1 diabetes mellitus (IDDM) is a chronic autoimmune disease caused by the selective destruction of pancreatic insulin-producing B cells (3). Autoimmunity comrnonly occurs when central or peripheral tolerance barriers are broken down, allowing the activation of self-reactive T cells (4). Recently, Thi 7 immunity has been reported to be correlated with IDDM (5). We describe here a case of NL associated with IDDM and demonstrate irnmunohistochemical staining for granuloma-forming cells, especially focusing on IL-17-producing cells and CD163* proinflammatory macrophages.
DOI：
10.1038/jid.2010.165
发表时间：
2010-10
期刊：
The Journal of investigative dermatology
影响因子：
--
作者：
通讯作者：
--