Albanesi Cristina, De Pità Ornella, Girolomoni Giampiero
Laboratory of Immunology and Allergology, Istituto Dermopatico dell'Immacolata (IDI)-IRCCS, Rome, Italy.
Clin Dermatol. 2007 Nov-Dec;25(6):581-8. doi: 10.1016/j.clindermatol.2007.08.013.
Psoriasis is a chronic inflammatory skin disease characterized by exaggerated keratinocyte proliferation. Current paradigm indicates that psoriasis is driven by T cell-mediated immune responses targeting keratinocytes. However, psoriasis cannot be explained solely on the basis of T-cell activation, and it is likely that intrinsic alterations in epidermal keratinocytes play a very relevant role in disease expression. In particular, keratinocytes may be important in initiating, sustaining, and amplifying the inflammatory responses by expressing molecules involved in T-cell recruitment, retention, and activation. Keratinocytes are also a relevant source of growth factors for angiogenesis. Finally, intrinsic defects in cytokine and growth factor signaling in keratinocytes may be responsible for their aberrant hyperproliferation and differentiation to T cell-derived signals. Other skin resident cells such as fibroblasts, mast cells, and endothelial cells also contribute to psoriasis pathogenesis by expressing molecules involved in T-cell recruitment and activation.
银屑病是一种慢性炎症性皮肤病,其特征为角质形成细胞过度增殖。目前的范式表明,银屑病是由针对角质形成细胞的T细胞介导的免疫反应驱动的。然而,银屑病不能仅基于T细胞活化来解释,表皮角质形成细胞的内在改变很可能在疾病表现中发挥非常重要的作用。特别是,角质形成细胞可能通过表达参与T细胞募集、滞留和活化的分子,在启动、维持和放大炎症反应中起重要作用。角质形成细胞也是血管生成生长因子的重要来源。最后,角质形成细胞中细胞因子和生长因子信号传导的内在缺陷可能是其异常过度增殖和对T细胞衍生信号分化的原因。其他皮肤驻留细胞,如成纤维细胞、肥大细胞和内皮细胞,也通过表达参与T细胞募集和活化的分子,参与银屑病的发病机制。