Sleep, sleep deprivation and immune functions – Aktuelle Themen in der Psychoneuroimmunologie

Sleep regulates immune functions. The first half of nocturnal sleep in humans is predominated by slow wave sleep (SWS) that serves memory and recovery functions. In addition, slow wave sleep and the circadian system act in concert to enhance the release of growth hormone (GH) and prolactin and to suppress the release of cortisol and catecholamines. This unique endocrine milieu existing around midnight facilitates the production of pro-inflammatory cytokines like interleukin (IL)–12 by stimulated monocytes and dendritic cell precursors. GH, prolactin and IL–12 are endogenous adjuvants that promote T helper (Th) 1 immune responses. Accordingly, sleep versus wakefulness in the night following a morning vaccination increases the amount of antigen-specific Th1 cells and Th1 dependent antibodies. Prolonged sleep loss in turn is associated with immunodeficiency and with a shift of the Th1/Th2 cytokine balance towards Th2, not only in sleep restriction experiments but also in clinical conditions like insomnia or depression. Moreover, sustained sleep loss increases the unstimulated, spontaneous release of pro-inflammatory cytokines like IL–6, resulting in a stress-like inflammatory response. This systemic low-grade inflammation is related to daytime fatigue and impacts metabolic and atherosclerotic pathways. In sum, the immunological consequences of sleep loss, i.e., immunodeficiency and inflammation likely contribute to the strong relationship between short sleep duration and increased all-cause mortality.

Antigen presenting cells - Sleep - T cells - circadian - cytokines - immune