A schematic representation of the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous interaction with the cutaneous immune system. Stress signals induce release of hormones, including corticotropin-releasing hormone (CRH) from the paraventricular nucleus (PVN) of the hypothalamus. CRH induces adrenocorticotropic hormone (ACTH) release from the anterior pituitary [20]. In turn, ACTH regulates glucocorticoid secretion from the adrenal cortex [22]. Cortisol has several functions including negative feedback of the hypothalamus and anterior pituitary and induces epinephrine and norepinephrine from the adrenal medulla [23]. Glucocorticoids, such as cortisol, as well as epinephrine and norepinephrine may enhance cutaneous immune responses at low concentrations and suppress immune responses at high concentrations [5, 28]. Stress signals also stimulate the locus coeruleus (LC) norepinephrine cells (NE) of the sympathetic nervous system [18]. Neuropeptide products of the sympathetic response (substance P (SP), calcitonin gene-related peptide (CGRP), and cutaneous nerve growth factor (NGF)) have been shown to be proinflammatory and anti-inflammatory dependent on the immune cell type [29–34]. There also exists a positive, reverberatory feedback loop between the HPA axis and LC-NE [18, 21]. Results show that HPA and sympathetic stress responses both modify the cutaneous immune response.