Sleep: The Immune System And The Immune System

Sleep is a necessary phenomenon that impacts many physiological processes in the human body, including immune system function. The immune system can be divided into two main categories: innate immunity and adaptive immunity1. The adaptive immune system is responsible for fighting against specific pathogens or antigens and a memory component is involved. Additionally, its response is longer than an innate immune response, upon its first exposure to said antigen or pathogen. In contrast, the innate immune system responds much faster, however there is no memory component involved. For instance, an individual could be exposed to a rhinovirus more than once and become sick each time. This is different than the adaptive immune response because once

Due to this down regulation, a subsequent decrease in cortisol, epinephrine, and norepinephrine occurs, which contributes to suppressed immune functions. In contrast, growth hormone, prolactin, melatonin, and leptin levels increase. These molecules act as pro-inflammatory signals to activate the immune system, aid in proliferation, differentiation, and generation of pro-inflammatory cytokines, including IL-1 and TNF-α4. At the beginning of slow-wave sleep (SWS), pro-inflammatory cytokines and Th1 cytokines increase, however there remains uncertainty as to why this occurs. One theory is that over the course of wakefulness, dangerous factors accumulate in the body, including reactive oxygen species (ROS), heat shock proteins (HSP), and nucleotides. These molecules are thought to be similar to microbial molecules such as lipopolysaccharide (LPS) and other toll-like receptor ligands that enhance the production of pro-inflammatory cytokines via antigen presenting cells (APCs). Additionally, immune cells have their own internal clocks that maintain periodic changes in pro-inflammatory cytokines4. In terms of specific cytokines, IL-1 and TNF-α have both been shown to increase NREM sleep in animal studies. It is therefore intuitive that through inactivation or interference with the normal action of these two cytokines, spontaneous NREM sleep is decreased. For instance, by preventing the activation of IL-1 by cleavage of its inactive form, NREM sleep is reduced3. It is also important to note that high levels of IL-1 inhibit sleep, which could be due to a feedback loop involving corticotropin-releasing hormone (CRH) stimulation by IL-1. In terms of immune regulation, IL-1 and TNF-α induce activation of nuclear factor kappa B (NFκB), a transcription factor that has been found to be associated with substances that regulate