Experiencing a stressful situation, as perceived by the brain, results in the stimulation of the hypothalamic–pituitary–adrenal (HPA) axis and the sympathetic–adrenal–medullary (SAM) axis. The production of adrenocorticotropic hormone by the pituitary gland results in the production of glucocorticoid hormones. The SAM axis can be activated by stimulation of the adrenal medulla to produce the catecholamines adrenaline and noradrenaline, as well as by 'hard-wiring', through sympathetic-nervous-system innervation of lymphoid organs.
Leukocytes have receptors for stress hormones that are produced by the pituitary and adrenal glands and can be modulated by the binding of these hormones to their respective receptors. In addition, noradrenaline produced at nerve endings can also modulate immune-cell function by binding its receptor at the surface of cells within lymphoid organs. These interactions are bidirectional in that cytokines produced by immune cells can modulate the activity of the hypothalamus. APC, antigen-presenting cell; IL-1, interleukin-1; NK, natural killer.
FULL PUBLISHED PAPER
source: Nature Reviews
Stress-induced immune dysfunction: implications for health
Ronald Glaser and Janice K. Kiecolt-Glaser
Nature Reviews Immunology 5, 243-251 (March 2005)