Effects of poor sleep on the immune cell landscape as assessed by single-cell analysis

TLDR

Poor sleep is a growing public health issue linked to increased disease risk. We employed mass cytometry and single‑cell RNA sequencing to generate a comprehensive human immune cell landscape in the context of poor sleep. The study profiled immune cell subsets, gene signatures, enriched pathways, transcriptional regulatory networks, and intercellular interactions. Staying up increased T and plasma cell frequencies and autoimmune markers in CD4⁺ T and B cells, reduced cytotoxic cell differentiation and activity, altered myeloid subset distribution, and promoted inflammation and cellular senescence, indicating a predisposition to infection and tumor development.

Abstract

Abstract Poor sleep has become an important public health issue. With loss of sleep durations, poor sleep has been linked to the increased risks for diseases. Here we employed mass cytometry and single-cell RNA sequencing to obtain a comprehensive human immune cells landscape in the context of poor sleep, which was analyzed in the context of subset composition, gene signatures, enriched pathways, transcriptional regulatory networks, and intercellular interactions. Participants subjected to staying up had increased T and plasma cell frequency, along with upregulated autoimmune-related markers and pathways in CD4 + T and B cells. Additionally, staying up reduced the differentiation and immune activity of cytotoxic cells, indicative of a predisposition to infection and tumor development. Finally, staying up influenced myeloid subsets distribution and induced inflammation development and cellular senescence. These findings could potentially give high-dimensional and advanced insights for understanding the cellular and molecular mechanisms of pathologic conditions related to poor sleep.