Inducible bronchus-associated lymphoid tissue (iBALT) in patients with pulmonary complications of rheumatoid arthritis
Inducible bronchus-associated lymphoid tissue (iBALT) in patients with pulmonary complications of rheumatoid arthritis
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DOI：
10.1172/jci28756
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发表时间：
2006-12-01
影响因子：
15.9
通讯作者：
Randall, Troy D.
中科院分区：
文献类型：
--
作者：
Rangel-Moreno, Javier;Hartson, Louise;Randall, Troy D.
支气管相关淋巴组织（BALT）最初被描述为某些物种肺中的粘膜淋巴器官。然而，虽然未处理小鼠和人类的肺通常缺乏BALT，但小鼠的肺部感染导致诱导型BALT（iBALT）的发展，其位于整个肺的支气管周围、血管周围和间质区域。在这里，我们调查了是否在各种间质性肺疾病患者中形成iBALT。我们发现，虽然iBALT可以在患有多种疾病的患者的肺部发现，但发育良好的iBALT在RA和干燥综合征的肺部并发症患者中最常见。在这些患者中，iBALT由含有生发中心和滤泡树突状细胞的大量B细胞滤泡组成。在B细胞滤泡周围有一个松散的T细胞区，而在B细胞处有毛细血管和高内皮微静脉。T细胞界面。淋巴组织趋化因子如CXCL 13和CCL 21，以及参与RA免疫病理学的分子如TNF家族的B细胞活化因子（BAFF）、ICOS配体和类光素的表达增加，与更发育良好的iBALT相关。最后，iBALT的存在与RA患者肺组织损伤相关，表明iBALT参与局部RA发病机制。
Bronchus-associated lymphoid tissue (BALT) was originally described as a mucosal lymphoid organ in the lungs of some species. However, while the lungs of naive mice and humans typically lack BALT, pulmonary infection in mice leads to the development of inducible BALT (iBALT), which is located in peribronchial, perivascular, and interstitial areas throughout the lung. Here we investigated whether iBALT forms in patients with a variety of interstitial lung diseases. We show that while iBALT can be found in the lungs of patients suffering from multiple diseases, well-developed iBALT is most prevalent in patients with pulmonary complications of RA and Sjogren syndrome. In these patients, iBALT consisted of numerous B cell follicles containing germinal centers and follicular dendritic cells. A loosely defined T cell area surrounded the B cell follicles while lymphatics and high endothelial venules were found at the B cell./T cell interface. Increased expression of lymphoid-organizing chemokines, such as CXCL13 and CCL21, as well as molecules involved in the immunopathology of RA, such as B cell-activating factor of the TNF family (BAFF), ICOS ligand, and lymphotoxin, correlated with more well-developed iBALT. Finally, the presence of iBALT correlated with tissue damage in the lungs of RA patients, suggesting that iBALT participates in local RA pathogenesis.