ECM1 controls TH2 cell egress from lymph nodes through re-expression of S1P1
ECM1 controls TH2 cell egress from lymph nodes through re-expression of S1P1
复制标题
ECM1 通过 S1P1 的重新表达控制 Th2 细胞从淋巴结的流出
DOI：
10.1038/ni.1983
复制
发表时间：
2011-02-01
影响因子：
30.5
通讯作者：
Sun, Bing
中科院分区：
文献类型：
--
作者：
Li, Zhenhu;Zhang, Yuan;Sun, Bing
2型辅助性T细胞（T（H）2）与过敏和哮喘密切相关。在这里，我们证明，细胞外基质蛋白-1（ECM 1）是高度和选择性地表达在T（H）2细胞。ECM 1缺乏导致T（H）2反应受损，并减少体内过敏性气道炎症。功能分析表明，尽管ECM 1缺陷细胞的T（H）2极化未受损，但这些细胞在迁移方面存在缺陷，并保留在外周淋巴器官中。这与KLF 2和S1 P表达减少有关（1）。我们还发现，ECM 1可以直接结合白细胞介素-2（IL-2）受体，抑制IL-2信号传导并激活S1 P（1）表达。我们的数据确定了ECM 1通过控制KLF 2和S1 P（1）表达来调节T（H）2细胞迁移的一种以前未知的功能。
Type 2 helper T cells (T(H)2) are critically involved in allergies and asthma. Here we demonstrate that extracellular matrix protein-1 (ECM1) is highly and selectively expressed in T(H)2 cells. ECM1 deficiency caused impaired T(H)2 responses and reduced allergic airway inflammation in vivo. Functional analysis demonstrated that although the T(H)2 polarization of ECM1-deficient cells was unimpaired, these cells had a defect in migration and were retained in peripheral lymphoid organs. This was associated with reduced expression of KLF2 and S1P(1). We also found that ECM1 could directly bind the interleukin-2 (IL-2) receptor to inhibit IL-2 signaling and activate S1P(1) expression. Our data identify a previously unknown function of ECM1 in regulating T(H)2 cell migration through control of KLF2 and S1P(1) expression.