| Abstrakt: |
Lymphoid organs receive extensive sympathetic and peptidergic/sensory innervation. Neurotransmitters and neuropeptides, released by the sympathetic and peptidergic nerve fibers in the vicinity of immunocompetent cells, and circulating epinephrine, secreted by the adrenal medulla affect major immune functions such as secretion of cytokines and antibodies, selection of T-helper (Th)1 or Th2 responses, lymphocyte activity, proliferation and traffic. Catecholamines (CAs), ATP, and adenosine inhibit the production of interleukin (IL-12), tumor necrosis factor (TNF)-α, and interferon (IFN)-ν, whereas they stimulate the production of IL-10. Thus, systemically, sympathetic neurotransmitters may induce a Th2 shift, and neuropeptide Y may further amplify this effect. In certain local responses, however, CAs induce IL-1, IL-6, IL-8, and TNF-α production; substance P upregulates IL-1, IL-12, and TNF-α production, whereas ATP via the P2X7 receptor may activate the posttranslational processing of IL-1β and IL-18. This might be aimed to localize the inflammatory response through induction of neutrophil and monocyte accumulation and stimulation of macrophage activity. Systemically, however, the activation of the sympathetic nervous system during an immune response may suppress Th1 responses, and, hence protect the organism from the detrimental effects of proinflammatory cytokines and other products of activated macrophages. Thus, a dysfunctional neural–immune interface may play a role in the pathogenesis of various common human immune-related diseases. [ABSTRACT FROM AUTHOR] |
