首页> 美国卫生研究院文献>The Journal of Experimental Medicine >Oral administration of lipopolysaccharides activates B-1 cells in the peritoneal cavity and lamina propria of the gut and induces autoimmune symptoms in an autoantibody transgenic mouse
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Oral administration of lipopolysaccharides activates B-1 cells in the peritoneal cavity and lamina propria of the gut and induces autoimmune symptoms in an autoantibody transgenic mouse

机译:口服脂多糖可激活肠腹膜腔和固有层的B-1细胞并在自身抗体转基因小鼠中诱发自身免疫症状

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摘要

About a half of the antierythrocyte autoantibody transgenic (autoAb Tg) mice, in which almost all B cells are detected in the spleen, lymph nodes, and Peyer's patches, but not in the peritoneal cavity, suffer from autoimmune hemolytic anemia. The occurrence of this disease is strongly linked to production of autoAb by activated peritoneal B-1 cells in the Tg mice. In this study, we have shown that oral administration of lipopolysaccharides (LPS) activated B-1 cells in the lamina propria of the gut as well as the peritoneal cavity in the healthy Tg mice and induced the autoimmune symptoms in all the Tg mice. The activation of peritoneal and lamina propria B-1 cells by enteric LPS is found not only in the anti-RBC autoAb Tg mice and normal mice but also in the aly mice which congenitally lack lymph nodes and Peyer's patches. These results suggest that B-1 cells in the two locations may form a common pool independent of Peyer's patches and lymph nodes, and can be activated by enteric thymus-independent antigens or polyclonal activators such as LPS. The induction of autoimmune hemolytic anemia in the Tg mice by enteric LPS through the activation of B-1 cells in the lamina propria of gut and in the peritoneal cavity suggests that B-1 cells and bacterial infection may play a pathogenic role in the onset of autoimmune diseases.
机译:大约一半的抗红细胞自身抗体转基因(autoAb Tg)小鼠患有自身免疫性溶血性贫血,其中几乎所有B细胞都在脾脏,淋巴结和Peyer斑块中检出,但在腹膜腔中未检出。这种疾病的发生与激活的腹膜B-1细胞在Tg小鼠中与autoAb的产生密切相关。在这项研究中,我们已经表明,在健康的Tg小鼠中,口服给予脂多糖(LPS)激活了肠道固有层以及腹膜腔中的B-1细胞,并在所有Tg小鼠中诱发了自身免疫症状。不仅在抗RBC autoAb Tg小鼠和正常小鼠中,而且在先天缺乏淋巴结和Peyer斑块的aly小鼠中发现了肠LPS对腹膜和固有层B-1细胞的激活。这些结果表明,这两个位置的B-1细胞可能形成独立于Peyer斑块和淋巴结的共同库,并且可以被不依赖胸腺的抗原或多克隆激活剂(例如LPS)激活。肠脂多糖通过激活肠道固有层和腹膜腔中的B-1细胞而在Tg小鼠中诱发自身免疫性溶血性贫血,表明B-1细胞和细菌感染可能在Bg的发病中起致病作用。自身免疫性疾病。

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