Ring J
Hautarzt. 1978 Dec;29(12):625-31.
Cyclic adenosin-3-5-monophosphate (c-AMP) plays a central role in regulating immune responses. Increased intracellular c-AMP has an inhibitory effect on release of histamine and other mediators from basophile leukocytes or mast cells as well as lysosomal enzymes from polymorphs. It depresses cell-mediated immune reactions and antibody formation. The hormonal factors which increase intracellular c-AMP are either of neuroendocrine origin (e.g. epinephrin) or inflammatory products (e.g. prostaglandins and histamine). This seems to be an endogenous mechanism of regulation which is able to stop immune or allergic reactions. Patients suffering from atopic diseases (asthma and/or atopic dermatitis) show a decreased reactivity to betaadrenergic stimuli. The defect is demonstrable in vitro in peripheral leukocytes which show a significantly smaller increase in intracellular c-AMP after betaadrenergic stimulation than normal leukocytes.
环磷腺苷（c-AMP）在调节免疫反应中起核心作用。细胞内c-AMP水平升高对嗜碱性白细胞或肥大细胞释放组胺及其他介质以及多形核白细胞释放溶酶体酶具有抑制作用。它还会抑制细胞介导的免疫反应和抗体形成。增加细胞内c-AMP的激素因子要么源自神经内分泌（如肾上腺素），要么是炎症产物（如前列腺素和组胺）。这似乎是一种内源性调节机制，能够阻止免疫或过敏反应。患有特应性疾病（哮喘和/或特应性皮炎）的患者对β-肾上腺素能刺激的反应性降低。这种缺陷在外周白细胞的体外实验中可以得到证实，与正常白细胞相比，β-肾上腺素能刺激后外周白细胞内c-AMP的增加明显较小。
