Iwakura Yoichiro, Ishigame Harumichi
Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
J Clin Invest. 2006 May;116(5):1218-22. doi: 10.1172/JCI28508.
IL-23 induces the differentiation of naive CD4(+) T cells into highly pathogenic helper T cells (Th17/Th(IL-17)) that produce IL-17, IL-17F, IL-6, and TNF-alpha, but not IFN-gamma and IL-4. Two studies in this issue of the JCI demonstrate that blocking IL-23 or its downstream factors IL-17 and IL-6, but not the IL-12/IFN-gamma pathways, can significantly suppress disease development in animal models of inflammatory bowel disease and MS (see the related articles beginning on pages 1310 and 1317). These studies suggest that the IL-23/IL-17 pathway may be a novel therapeutic target for the treatment of chronic inflammatory diseases.
白细胞介素-23可诱导初始CD4(+) T细胞分化为高致病性辅助性T细胞（Th17/Th(IL-17)），这些细胞可产生白细胞介素-17、白细胞介素-17F、白细胞介素-6和肿瘤坏死因子-α，但不产生干扰素-γ和白细胞介素-4。本期《临床研究杂志》上的两项研究表明，阻断白细胞介素-23或其下游因子白细胞介素-17和白细胞介素-6，而非白细胞介素-12/干扰素-γ途径，可显著抑制炎症性肠病和多发性硬化症动物模型中的疾病发展（见第1310页和1317页开始的相关文章）。这些研究表明，白细胞介素-23/白细胞介素-17途径可能是治疗慢性炎症性疾病的一个新的治疗靶点。
