Bidirectional interactions between antigen-bearing respiratory tract dendritic cells (DCs) and T cells precede the late phase reaction in experimental asthma: DC activation occurs in the airway mucosa but not in the lung parenchyma.
Bidirectional interactions between antigen-bearing respiratory tract dendritic cells (DCs) and T cells precede the late phase reaction in experimental asthma: DC activation occurs in the airway mucosa but not in the lung parenchyma.
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DOI：
10.1084/jem.20021328
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发表时间：
2003-07-07
期刊：
影响因子：
--
通讯作者：
Holt PG
中科院分区：
文献类型：
--
作者：
Huh JC;Strickland DH;Jahnsen FL;Turner DJ;Thomas JA;Napoli S;Tobagus I;Stumbles PA;Sly PD;Holt PG
哮喘气道黏膜对变应原的反应包括活化的2型辅助性T细胞和嗜酸性粒细胞的内流、短暂的气流阻塞和气道高反应性（AHR）。在这种炎症反应过程中瞬时T细胞活化的机制尚不清楚。我们目前的证据表明，这种反应是通过气道粘膜树突状细胞（AMDC）和T记忆细胞之间的双向相互作用进行调节。气溶胶攻击后，常驻AMDC获得抗原，并在与T记忆细胞同源相互作用后迅速成熟为有效的抗原呈递细胞（APC）。这一过程仅限于传导气道粘膜中的树突状细胞（DC），而在外周肺中未见。在24小时内，携带抗原的成熟DC从气道壁消失，在它们的觉醒中留下活化的白细胞介素2 R + T细胞和AHR。在24小时，携带抗原的活化DC出现在区域淋巴结中，表明从气道向前迁移。CD 86在AMDC上的瞬时上调伴随着这个过程，这可以通过将静息AMDC与T记忆细胞加抗原共培养来再现。AMDC的APC活性可被抗CD 86抗体部分抑制，提示CD 86可能在此过程中起积极作用和/或作为其他相关共刺激因子的替代物。这些发现提供了一个合理的模型，局部T细胞活化在病变部位的哮喘，这种炎症反应的短暂性。
The airway mucosal response to allergen in asthma involves influx of activated T helper type 2 cells and eosinophils, transient airflow obstruction, and airways hyperresponsiveness (AHR). The mechanism(s) underlying transient T cell activation during this inflammatory response is unclear. We present evidence that this response is regulated via bidirectional interactions between airway mucosal dendritic cells (AMDC) and T memory cells. After aerosol challenge, resident AMDC acquire antigen and rapidly mature into potent antigen-presenting cells (APCs) after cognate interactions with T memory cells. This process is restricted to dendritic cells (DCs) in the mucosae of the conducting airways, and is not seen in peripheral lung. Within 24 h, antigen-bearing mature DCs disappear from the airway wall, leaving in their wake activated interleukin 2R+ T cells and AHR. Antigen-bearing activated DCs appear in regional lymph nodes at 24 h, suggesting onward migration from the airway. Transient up-regulation of CD86 on AMDC accompanies this process, which can be reproduced by coculture of resting AMDC with T memory cells plus antigen. The APC activity of AMDC can be partially inhibited by anti-CD86, suggesting that CD86 may play an active role in this process and/or is a surrogate for other relevant costimulators. These findings provide a plausible model for local T cell activation at the lesional site in asthma, and for the transient nature of this inflammatory response.
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DOI：
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