Development of chronic colitis is dependent on the cytokine MIF
Development of chronic colitis is dependent on the cytokine MIF
复制标题
DOI：
10.1038/ni720
复制
发表时间：
2001-11-01
影响因子：
30.5
通讯作者：
Terhorst, C
中科院分区：
文献类型：
--
作者：
de Jong, YP;Abadia-Molina, AC;Terhorst, C
细胞因子巨噬细胞移动抑制因子(MIF)是由多种细胞在脂多糖(LPS)诱导下分泌的。由于结肠炎依赖于粘膜免疫系统和肠道细菌之间的相互作用，我们研究了MIF在实验性结肠炎中的作用。MIF基因缺陷的小鼠没有发生疾病，但用野生型天然免疫细胞重建MIF基因缺陷小鼠后，结肠炎得到了恢复。此外，确诊的结肠炎可以用抗MIF免疫球蛋白治疗。因此，小鼠结肠炎依赖于先天性免疫系统持续产生MIF。由于我们发现克罗恩病患者血浆MIF浓度升高，这些数据表明MIF是克罗恩病干预的新靶点。
The cytokine macrophage-migration inhibitory factor (MIF) is secreted by a number of cell types upon induction by lipopolysaccharide (LPS). Because colitis is dependent on interplay between the mucosal immune system and intestinal bacteria, we investigated the role of MIF in experimental colitis. MIF-deficient mice failed to develop disease, but reconstitution of MIF-deficient mice with wild-type innate immune cells restored colitis. In addition, established colitis could be treated with anti-MIF immunoglobulins. Thus, murine colitis is dependent on continuous MIF production by the innate immune system. Because we found increased plasma MIF concentrations in patients with Crohn's disease, these data suggested that MIF is a new target for intervention in Crohn's disease.