Abstract：
Sleep deprivation (SD) weakens the immune system and leads to increased susceptibility to infectious or inflammatory diseases. However, it is still unclear how SD affects humoral immunity. In the present study, sleep disturbance was conducted using an sleep deprivation instrument, and the bacterial endotoxin lipopolysaccharide (LPS) was used to activate the immune response. It was found that SD-pretreatment reduced LPS-induced IgG2b+ B cells and IgG2b isotype antibody production in lymphocytes of spleen. And, SD-pretreatment decreased the proportion of CD4+T cells, production of CD4+T cells derived TGF-β1 and its contribution in helping IgG2b production. Additionally, BMAL1 and CLOCK were selectively up-regulated in lymphocytes after SD. Importantly, BMAL1 and CLOCK deficiency contributed to TGF-β1 expression and production of IgG2b+ B cells. Thus, our results provide a novel insight to explain the involvement of BMAL1 and CLOCK under SD stress condition, and their roles in inhibiting TGF-β1 expression and contributing to reduction of LPS induced IgG2b production.
摘要：
睡眠剥夺（SD）会削弱免疫系统，并导致对传染病或炎性疾病的易感性增加。然而,尚不清楚SD如何影响体液免疫。在本研究中,睡眠障碍是使用睡眠剥夺工具进行的，细菌内毒素脂多糖（LPS）用于激活免疫应答。发现SD预处理减少了LPS诱导的IgG2bB细胞和脾淋巴细胞中IgG2b同种型抗体的产生。And,SD预处理降低了CD4+T细胞的比例，CD4+T细胞衍生的TGF-β1的产生及其在帮助IgG2b产生中的贡献。此外,SD后淋巴细胞中BMAL1和CLOCK选择性上调。重要的是,BMAL1和CLOCK缺乏有助于TGF-β1的表达和IgG2bB细胞的产生。因此，我们的结果为解释SD应激条件下BMAL1和CLOCK的参与提供了新的见解，以及它们在抑制TGF-β1表达和减少LPS诱导的IgG2b产生中的作用。
