Description:
<jats:p><jats:bold><jats:sc>Abstract: </jats:sc></jats:bold> <jats:bold>It has long been postulated that stress can affect certain skin conditions, and there is increasing experimental evidence that the neuroendocrine system can directly participate in cutaneous inflammation. Neurohormones, such as glucocorticoids and catecholamines, can reach the skin through the bloodstream after activation of the hypothalamic–pituitary–adrenal axis and the sympathetic nervous system, respectively. Multiple neuropeptides, among them calcitonin gene–related peptide, α‐melanocyte stimulating hormone, pituitary adenylate cyclase–activating peptide, substance P, vasoactive intestinal peptide, and norepinephrine, may be released by cutaneous nerves or resident and infiltrating cells within the skin. Systemic neuromediators and cutaneous nerves can influence a number of target cells within the skin, among them Langerhans cells. Most of the experimental evidence to date indicates a suppressive effect of the neurohormones and neuropeptides on Langerhans cell function and cutaneous inflammation, but it has become evident lately that the timing of exposure to a stimulus is critical to the outcome of the immune response. Thus, administration of a stress hormone or exposure to a stressor before the dendritic cell (DC) encounters an antigen (Ag) may diminish the immune response toward that Ag, while a stressor may enhance immune function when acting on a maturing DC or before reexposure to the Ag. The neuroendocrine regulation of skin DCs is a complex system allowing for a quick adaptation to various stressors. Such a system, originally evolved to defend the organism against invading pathogens and maintain homeostasis, may under certain conditions become unbalanced and ultimately exacerbate cutaneous inflammation.</jats:bold> </jats:p>