Popular wisdom says sleep helps you fight off illness, and over the last few decades neuroimmunology has accumulated surprisingly strong evidence for it. Separating sleep from the circadian rhythm it rides on is difficult, which makes the specific question hard. Besedovsky, Lange and Born review what the immune system actually does across a night. Is it resting too?
No, it is doing different work. Undifferentiated and pro-inflammatory cytokine production peak during early nocturnal sleep, while cells with immediate effector functions, such as cytotoxic , and anti-inflammatory cytokine activity peak in daytime wakefulness. Comparing a night of sleep with twenty-four hours awake suggests sleep helps T cells leave the bloodstream and redistribute, possibly to .
Sleep and the circadian system both exert a strong regulatory influence on immune function, and over the last few decades a systems approach in neuroimmunology has built strong evidence that sleep enhances immune defense. The difficulty throughout is that the two influences are hard to pull apart, since one runs inside the other.
Across a normal cycle, different parts of the immune system peak at different hours. Numbers of undifferentiated naive T cells and the production of pro-inflammatory cytokines rise during early nocturnal sleep. Circulating numbers of cells with immediate effector functions, such as cytotoxic natural killer cells, and anti-inflammatory cytokine activity instead peak during daytime wakefulness.
Comparing a night of sleep against a full twenty-four hours of wakefulness gives a sharper picture. Those comparisons suggest sleep helps T cells leave the bloodstream, with possible redistribution to lymph nodes. They also point to a selective boost to cytokines promoting the interaction between antigen presenting cells and T helper cells, interleukin-twelve among them.
The vaccination result is the one that ties it together. Sleep on the night after experimental vaccination against hepatitis A produced a strong and persistent increase in antigen-specific T helper cells and antibody titres. The authors read all of this as a specific role for sleep in forming immunological memory. They tie it particularly to and the endocrine milieu that accompanies it: high growth hormone and prolactin, low cortisol and catecholamines.
wat. Daytime immunity is the patrol. Night-time immunity looks more like filing what the patrol found.
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It reframes what sleep is for. If immunological memory forms preferentially during slow wave sleep, then losing a night is not only tiring but costly in a specific way.
How do we know?
An invited review in Pflugers Archiv gathers studies of the normal sleep-wake cycle, experiments comparing nocturnal sleep against a full day and night awake, and vaccination experiments that followed antibody responses over time.
What is still unknown
The influence of sleep is difficult to separate entirely from that of the circadian system, which the authors state plainly. Much of the case rests on comparisons against sleep deprivation rather than on direct manipulation of one factor.
Learn something?
Where to next
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