胫前黏液性水肿发生发展机制的研究进展

Advances in the mechanisms of initiation and progression of pretibial myxedema

在自身免疫性甲状腺疾病背景下,循环自身抗体与成纤维细胞上自身抗原结合,产生IL～16和活化后可调节的正常T细胞表达并可能分泌的因子,趋化吸引CD4＋T淋巴细胞.浸润T细胞活化成纤维细胞,分泌IL-6、8和巨噬细胞趋化蛋白-1,吸引炎性细胞浸润,形成血管周围炎.自身抗体、细胞因子与浸润T细胞使成纤维细胞合成过多透明质酸,发生黏液性水肿.局部创伤、感染可能起触发作用.持续大量细胞因子和透明质酸刺激成纤维细胞增殖并分化为肌成纤维细胞,过度合成细胞外基质,真皮纤维化,皮肤硬化.

In autoimmune thyroid diseases, circulating autoantibodies bind to autoantigens on dermal fibroblasts. IL-16 and RANTES （regulated on activation, normal T cell expressed and secreted） produced by the autoantibody-binding fibroblasts chemoattract CD4 ＋ T lymphocytes to infiltrate nnto the dermis. The infiltrated CD4＋ T cells interact with and activate the fibroblasts to produce interleukin （IL）-6, IL-8 and macrophage chemotactic protein （MCP）-1, which recruit more inflammatory leukocytes and result in perivasculitis. In these processes, large amounts of cytokines, autoantibodies, together with the interactions between T lymphocytes and fibroblasts lead to the accumulation of hyalumnan in dermis, which results in pretibial myxedema. Local trauma or infection may initiate the above immunological processes. Large amounts of cytokines and hyaluronan persistently stimulate the fibroblasts to propagate and differentiate into myofibroblasts, as well as to overproduce extracellular matrices, which together causes dermal fibrosis and cutaneous sclerosis.