B-1a B cells that link the innate and adaptive immune responses are lacking in the absence of the spleen.
B-1a B cells that link the innate and adaptive immune responses are lacking in the absence of the spleen.
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DOI：
10.1084/jem.20011140
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发表时间：
2002-03-18
影响因子：
15.3
通讯作者：
Carsetti, Rita
中科院分区：
文献类型：
--
作者：
Wardemann, Hedda;Boehm, Thomas;Dear, Neil;Carsetti, Rita
脾切除的个体易于被包裹的细菌压倒性感染，并且小鼠脾切除增加了对链球菌感染的易感性，但脾保护免受此类感染的确切机制尚不清楚。使用先天性无脾小鼠作为模型，我们表明，脾脏是必不可少的B-1a细胞，一个B细胞群体，与先天免疫系统合作，以控制早期细菌和病毒的生长。野生型小鼠的脾切除术进一步证明脾对于B-1a细胞的存活也是重要的。转移实验表明，缺乏这些细胞，而不是缺乏脾脏本身，是与无法安装一个快速的免疫反应，对链球菌多糖。因此，脾脏缺失和相关的链球菌感染易感性增加与B-1a B细胞缺失相关。这些发现揭示了脾脏在产生和维持B-1a B细胞库中迄今未知的作用。
Splenectomized individuals are prone to overwhelming infections with encapsulated bacteria and splenectomy of mice increases susceptibility to streptococcal infections, yet the exact mechanism by which the spleen protects against such infections is unknown. Using congenitally asplenic mice as a model, we show that the spleen is essential for the generation of B-1a cells, a B cell population that cooperates with the innate immune system to control early bacterial and viral growth. Splenectomy of wild-type mice further demonstrated that the spleen is also important for the survival of B-1a cells. Transfer experiments demonstrate that lack of these cells, as opposed to the absence of the spleen per se, is associated with an inability to mount a rapid immune response against streptococcal polysaccharides. Thus, absence of the spleen and the associated increased susceptibility to streptococcal infections is correlated with lack of B-1a B cells. These findings reveal a hitherto unknown role of the spleen in generating and maintaining the B-1a B cell pool.