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The study of basic interactions among the nervous, endocrine, and immune systems during development, homeostasis, and host defense responses to injury. In its clinical aspects, neuroimmunology focuses on diseases of the nervous system, such as myasthenia gravis and multiple sclerosis, which are caused by pathogenic autoimmune processes, and on nervous system manifestations of immunological diseases, such as primary and acquired immunodeficiencies. See Autoimmunity, Immunological deficiency
Neuroimmune interactions are dependent on the expression of at least two structural components: immunocytes must display receptors for nervous system-derived mediators, and the mediators must be able to reach immune cells in concentrations sufficient to alter migration, proliferation, phenotype, or secretory or effector functions. More than 20 neuropeptide receptors have been identified on immunocompetent cells.
It has been found that stimuli derived from the nervous system could affect the course of human disease. The onset or progression of tumor growth, infections, or chronic inflammatory diseases, for example, could be associated with traumatic life events or other psychosocial variables such as personality types and coping mechanisms. More direct indications of the influence of psychosocial factors on immune function have been provided by findings that cellular immunity can be impaired in individuals who are exposed to unusually stressful situations, such as the loss of a close relative. See Cellular immunology
During responses to infection, trauma, or malignancies, cells of the immune system produce some cytokines in sufficiently high quantities to reach organs that are distant from the site of production. These cytokines are known to act on the nervous system. Fever is the classic example of changes in nervous system function induced by products of the immune system; interleukin 1, which is produced by monocytes after stimulation by certain bacterial products, binds to receptors in the hypothalamus and evokes changes via the induction of prostaglandins. Interleukin 1 also induces slow-wave sleep. Both fever and sleep may be regarded as protective behavioral changes. See Endocrine system (vertebrate), Immunology, Nervous system (vertebrate), Neurosecretion