摘要
银屑病发病机制的神经免疫调节是在一定的遗传背景基础上 ,神经系统通过分布于皮肤的神经末梢释放神经肽作用于皮肤的免疫细胞 (包括Langerhans细胞、T淋巴细胞、单核巨噬细胞和内皮细胞等 ) ,影响这些细胞的生物学功能。其中T淋巴细胞是银屑病发病过程中的主要效应细胞 ,由于T淋巴细胞调节的紊乱 ,导致T细胞表型和功能的变化 ,释放相关的细胞因子 ,可能诱导了银屑病表皮角朊干细胞增殖状态的病理性改变 ,使角朊细胞过度增殖、表皮可凋亡的角朊细胞异常分化 ,从而诱发银屑病发病机制的神经免疫调节紊乱的病变过程。目前研究表明 ,在与皮肤有关的神经递质中 ,降钙素基因相关肽 (calcitoningene relatedpeptide ,CGRP)是与皮肤免疫细胞联系较密切的神经肽 ,能刺激人皮肤微血管内皮细胞分泌趋化因子 ,影响免疫细胞的迁移。同时 ,在银屑病斑块型皮损内 ,CGRP的分泌释放增加 ,并与皮损表皮的Langerhans细胞密切接触 。
The neuroimmunolmodulation of psoriatic pathogenesis is based on the some genetic background. The subcutaneous nerve fiber erels release neuropeptides which have modulating effects on the Langerhans cell , T lymphocyte , monocyte/macrophage and endotheliocyte. T lymphocyte is main effective cell in psoriatic pathogenesis . T lymphocytes release cytokines to induce the pathogenetic change of psoriatic epidermal stem cell hyperplasia, as well as to increase keratinocyte proliferation and lead abnormal differentiation of these apoptotic cells that end their life cycles as corneocytes, resulting in abnormal neuroimmunologic regulation of psoriatic pathogenesis. Recently some research work show that cacitonin gene related peptide (CGRP) closely contact with the cutaneou immune cells. CGRP stimulate the human dermal microvascular endothelial cell (HDMEC) to release chemokine. There are increased quantity of CGRP in psoriatic plaque lesions, and CGRP contact with Langerhans cell in the epidermal of psoriatic lesions. The results indicate CGRP may play a certain of role in the pathogenosis of psoriatic plaque lesion existance and development.
出处
《北京医科大学学报》
CSCD
2000年第4期362-365,共4页
Journal of Peking University(Health Sciences)
关键词
银屑病
病因学
神经免疫调节
T细胞
发病机制
Psoriasis/etiol
Neuroimmunomodulation
T lymphocytes/drug eff
Neuropeptides/pharmacol
