Heijnen C J, Rouppe van der Voort C, Wulffraat N, van der Net J, Kuis W, Kavelaars A
Department of Immunology, University Hospital for Children and Youth Het Wilhelmina Kinderziekenhuis, Utrecht, The Netherlands.
J Neuroimmunol. 1996 Dec;71(1-2):223-6. doi: 10.1016/s0165-5728(96)00125-7.
During the last decade it has been shown that the central nervous system can influence the immune system. In healthy individuals, catecholamines can inhibit the production of pro-inflammatory cytokines like interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) via interaction with beta 2-adrenergic receptors. In contrast, we show here that catecholamines can stimulate the production of the interleukin-6 (IL-6) in children with the chronic inflammatory disease polyarticular juvenile rheumatoid arthritis (JRA). The induction of IL-6 is mediated by triggering of alpha 1-adrenergic receptors on peripheral blood leucocytes of the patients with polyarticular JRA. Functional alpha 1-adrenergic receptors are absent on leukocytes of normal donors and on leukocytes of patients with the oligoarticular form of the disease.
在过去十年中,已表明中枢神经系统可影响免疫系统。在健康个体中,儿茶酚胺可通过与β2-肾上腺素能受体相互作用,抑制促炎细胞因子如白细胞介素-6(IL-6)和肿瘤坏死因子α(TNF-α)的产生。相比之下,我们在此表明,儿茶酚胺可刺激患有慢性炎症性疾病多关节型幼年类风湿性关节炎(JRA)的儿童产生白细胞介素-6(IL-6)。IL-6的诱导是通过触发多关节型JRA患者外周血白细胞上的α1-肾上腺素能受体介导的。正常供体的白细胞以及寡关节型疾病患者的白细胞上不存在功能性α1-肾上腺素能受体。