Sleep deprivation reduced LPS-induced IgG2b production by up-regulating BMAL1 and CLOCK expression

  • Impact factors: 3.1
  • Publication: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
  • Author:Chen Xing, Bing Zhai, Yifan Zhang, Ying Fang, Min Zhang, Chongchong Zhang, Wei Wang, Mengnan Ding, Xin Huang, Beifen Shen, Renxi Wang, Lun Song
  • DOI citation-doi:10.1016/j.bbrc.2023.149326
  • Date:2023-11-25

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.

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