Kavelaars A, Eggen B J, De Graan P N, Gispen W H, Heijnen C J
Department of Pediatric Immunology, University Hospital for Children and Youth, Het Wilhelmina Kinderziekenhuis, The Netherlands.
Eur J Immunol. 1990 Apr;20(4):943-5. doi: 10.1002/eji.1830200435.
The neuropeptide beta-endorphin can modulate the response of T and B cells to mitogenic or antigenic stimulation. In the present report we describe a novel mechanism by which beta-endorphin can interfere with T cell activation. It is shown here that beta-endorphin can modulate the phorbol ester-induced phosphorylation of the gamma chain of the CD3 complex. The effect of beta-endorphin is dose dependent and appears to be mediated via interaction of beta-endorphin with an opiate receptor on lymphocytes. Evidence is presented that the modulatory effect of beta-endorphin is specific for the phosphorylation of the CD3 gamma chain. beta-Endorphin does not affect the phosphorylation of total cell protein, nor does it have any effect on the phosphorylation of the CD4 determinant on T cells. The possible consequence of a change in CD3 gamma chain phosphorylation is discussed.
神经肽β-内啡肽可调节T细胞和B细胞对有丝分裂原或抗原刺激的反应。在本报告中，我们描述了β-内啡肽干扰T细胞活化的一种新机制。本文表明，β-内啡肽可调节佛波酯诱导的CD3复合物γ链的磷酸化。β-内啡肽的作用呈剂量依赖性，似乎是通过β-内啡肽与淋巴细胞上的阿片受体相互作用介导的。有证据表明，β-内啡肽的调节作用对CD3γ链的磷酸化具有特异性。β-内啡肽不影响总细胞蛋白的磷酸化，对T细胞上CD4决定簇的磷酸化也没有任何影响。文中讨论了CD3γ链磷酸化变化可能产生的后果。
