Cutting edge: Th2 cell trafficking into the allergic lung is dependent on chemoattractant receptor signaling
Cutting edge: Th2 cell trafficking into the allergic lung is dependent on chemoattractant receptor signaling
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DOI：
10.4049/jimmunol.169.2.651
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发表时间：
2002-07-15
影响因子：
4.4
通讯作者：
Luster, AD
中科院分区：
文献类型：
--
作者：
Mathew, A;Medoff, BD;Luster, AD
Th2细胞被招募到肺部，在那里它们介导哮喘表型。由于调节Th2细胞转运的分子机制尚不清楚，我们试图确定Th2细胞转运进入肺部是否由galphai偶联的化学引诱剂受体介导。我们在这里表明，与未处理的Th2细胞相比，百日咳毒素处理的Th2细胞在银攻击后不能进入肺、气道或淋巴结，因此不能在体内诱导过敏性炎症。然而，百日咳毒素处理的Th2细胞是功能性细胞，当直接注入小鼠的气道时，绕过它们通往肺部的需要，能够诱导气道嗜酸性炎症。这些研究最终证明Th2细胞进入肺部是一个依赖于化学引诱剂受体的活跃过程。
Th2 cells are recruited to the lung where they mediate the asthma phenotype. Since the molecular mechanisms regulating Th2 cell trafficking remain unknown, we sought to determine whether trafficking of Th2 cells into the lung is mediated by Galphai-coupled chemoattractant receptors. We show here that in contrast to untreated Th2 cells, pertussis toxin-treated Th2 cells were unable to traffic into the lung, airways, or lymph nodes following Ag challenge and therefore were unable to induce allergic inflammation in vivo. Pertussis toxin-treated Th2 cells were functional cells, however, and when directly instilled into the airways of mice, bypassing their need to traffic to the lung, were able to induce airway eosinophilic inflammation. These studies conclusively demonstrate that trafficking of Th2 cells into the lung is an active process dependent on chemoattractant receptors.