Sleep restriction alters the temporal expression of major histocompatibility complex class II molecules in murine lymphoid tissues

Folic Acid Supplementation Suppresses Sleep Deprivation-Induced Telomere Dysfunction and Senescence-Associated Secretory Phenotype (SASP)

“…During sleep, most of the body's systems are in a state of synthesis, helping to restore the immune, nervous, skeletal, and muscular systems, which are important to maintain emotion, memory, and cognitive functions [1]. However, sleep deprivation (SD) or chronic sleep restriction has become a relevant health problem caused by social factors, such as wide usage of electronic products and networks, night-shift work or overtime work schedules, and chronic diseases [2][3][4]. Previous studies have shown that sleep deprivation leads to a number of aging-related diseases, including chronic inflammation, Alzheimer's disease, and cardiovascular disease [5][6][7][8][9][10] and even causes mortality when individuals are severely deprived of sleep [11,12].…”

The temporal expression pattern of classical MHC class I in sleep-restricted mice: Generalizations and broader implications

“…Noteworthy, these secondary lymphoid organs have gained research attention in view of their central role in antigen presentation and priming NKCs, dendritic cells, thereby orchestrating between innate and immune responses. In one study, we described the role of sleep restriction in promoting a state of inflammation possibly mediated by MHC class II-dependent mechanisms ( Ghanem et al, 2019 ). Therefore, knowing that no information is available about circadian regulation of MHC class I in sleep restricted states, we designed the present study with the following aims: 1) to assess the temporal expression profile of MHC class I in the axillary lymph nodes and spleen under normal and acute sleep restriction in mice and 2) to examine whether 3–4 days of recovery following restriction might have potential effects on MHC class I timely expression.…”