How (and why) the immune system makes us sleep

Abstract
Serotonin promotes wakefulness but is necessary for sleep. Cytokines, such as interleukin 1 (IL-1) and tumor necrosis factor, are involved in regulating physiological non-rapid eye movement (NREM) sleep. IL-1 contributes to the regulation of NREM sleep in part through interactions with serotonin. Interactions between IL-1 and serotonin are amplified during infection, and sleep is altered. During infection, NREM sleep is fragmented and REM sleep is suppressed. Changes induced in sleep architecture by infectious agents support the generation of fever, and fever imparts survival value.