Yamamoto Toshiyuki
Department of Dermatology, Tokyo Medical University, Tokyo, Japan.
Int Arch Allergy Immunol. 2006;140(4):345-56. doi: 10.1159/000094242. Epub 2006 Jun 27.
Scleroderma is a connective tissue disease with unknown etiology characterized by excessive deposition of extracellular matrix in the skin. Cellular infiltrates of certain immune cells and proinflammatory mediators are suggested to play a crucial role in cutaneous fibrosis, forming complicated networks between fibroblasts and immune cells via cell-cell communications. Tissue-selective trafficking of leukocytes is mediated by combinations of adhesion molecules and chemokines. Recent studies have shown that an increase in proinflammatory chemokines has been associated with the initiation and/or development of skin fibrosis/sclerosis, suggesting that chemokines and their receptors may be important mediators of inflammation and fibrosis in scleroderma. This review will focus on the roles of chemokines and their receptors during the process of cutaneous sclerosis and will also provide a current insight into the potential mechanisms of scleroderma.
硬皮病是一种病因不明的结缔组织疾病,其特征是皮肤中细胞外基质过度沉积。某些免疫细胞和促炎介质的细胞浸润被认为在皮肤纤维化中起关键作用,通过细胞间通讯在成纤维细胞和免疫细胞之间形成复杂的网络。白细胞的组织选择性运输由粘附分子和趋化因子共同介导。最近的研究表明,促炎趋化因子的增加与皮肤纤维化/硬化的起始和/或发展有关,这表明趋化因子及其受体可能是硬皮病炎症和纤维化的重要介质。本综述将聚焦趋化因子及其受体在皮肤硬化过程中的作用,并对硬皮病的潜在机制提供当前的见解。