Department of Dermatology, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, 113-8519, Japan.
Acta Derm Venereol. 2012 Jul;92(4):367-71. doi: 10.2340/00015555-1285.
Psoriasis is a chronic skin disease mediated by Th17 and/or Th1 cells. Tim-3 is a cell surface molecule preferentially expressed on Th17 and Th1 cells. The interaction of Tim-3 with Tim-3 ligand inhibits cytokine production. To assess whether T cells in psoriasis have functional abnormalities, expression of cell surface Tim-3 on blood T cells producing interleukin-17 (Th17/Tc17 cells) or interferon-γ (Th1/Tc1 cells) was examined by flow cytometry. Psoriasis patients had higher numbers of Th17 and Tc17 cells, as well as Th1 and Tc1 cells, than healthy donors. However, Th17, Th1 and Tc1 cells in psoriasis did not efficiently express Tim-3 upon activation, compared with those from atopic dermatitis and healthy donors. Tim-3- cells showed more potent cytokine production than Tim-3+ cells. Impaired Tim-3 expression allows Th17, Th1 and Tc1 cells to escape from Tim-3-mediated negative regulatory systems and may contribute to the pathogenesis of psoriasis.
银屑病是一种由 Th17 和/或 Th1 细胞介导的慢性皮肤病。Tim-3 是一种优先表达于 Th17 和 Th1 细胞表面的细胞表面分子。Tim-3 与 Tim-3 配体的相互作用抑制细胞因子的产生。为了评估银屑病 T 细胞是否存在功能异常，通过流式细胞术检测产生白细胞介素-17（Th17/Tc17 细胞）或干扰素-γ（Th1/Tc1 细胞）的血液 T 细胞表面 Tim-3 的表达。与健康供体相比，银屑病患者的 Th17 和 Tc17 细胞以及 Th1 和 Tc1 细胞数量更高。然而，与特应性皮炎和健康供体相比，银屑病中的 Th17、Th1 和 Tc1 细胞在激活时并不有效地表达 Tim-3。Tim-3-细胞比 Tim-3+细胞产生更强效的细胞因子。Tim-3 表达受损使 Th17、Th1 和 Tc1 细胞逃脱 Tim-3 介导的负调节系统，可能有助于银屑病的发病机制。
