| First Author | Xing C | Year | 2024 |
| Journal | Biochem Biophys Res Commun | Volume | 691 |
| Pages | 149326 | PubMed ID | 38035406 |
| Mgi Jnum | J:343734 | Mgi Id | MGI:7566946 |
| Doi | 10.1016/j.bbrc.2023.149326 | Citation | Xing C, et al. (2023) Sleep deprivation reduced LPS-induced IgG2b production by up-regulating BMAL1 and CLOCK expression. Biochem Biophys Res Commun 691:149326 |
| abstractText | 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-beta1 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-beta1 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-beta1 expression and contributing to reduction of LPS induced IgG2b production. |
