The immune system and the pathogenesis of depression

http://bit.ly/2Kd6X0F

The immune, neural and psychological systems all interact with one another. One of the major communication pathways between the brain and the immune system is the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system. This pathway mediates our immune response to psychological factors such as stress, anxiety and other emotions. This bidirectional relationship between the brain and the immune system has led to the question about the role of the immune system in neuropathological processes.

Our immune system acts as the sensory organ when our body is confronted with pathogens. The immune system alerts the brain, and the rest of the body, to the presence of these pathogens by generating an immune response. The cells responsible for our immunity (T cells, B cells and mast cells) release cytokines in response to activation. Cytokines, such as interleukins and interferons, are peptides (proteins) that orchestrate the immune response. They are released both in the periphery as well as the brain during immune stimulation, and can affect neural, neuroendocrine, and behavioural functions.

In addition to standard physiological responses that we’re all probably used to such as fever, activation of the HPA axis also produces some behavioural changes. At one point or another, most of us would have had experiences that are referred to as ‘sickness behaviour’. This behaviour is exhibited by physically ill people and can present as depressed mood, anorexia, weight loss, sleepiness and altered sleep patterns, fatigue and retardation of motor activity, reduced interest in the physical and social environment, and impaired cognitive abilities. This behavioural response is considered to be an adaptive response to aid the recovery process, rather than being caused by the illness itself. This is essentially why we don’t go out and stay in bed when we’re ill — thus speeding up our recovery!