Impaired sympathetic influence on the immune response in patients with rheumatoid arthritis due to lymphocyte subset-specific modulation of beta 2-adrenergic receptors.

Impaired sympathetic influence on the immune response in patients with rheumatoid arthritis due to lymphocyte subset-specific modulation of beta 2-adrenergic receptors.
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DOI:
10.1093/rheumatology/36.12.1262
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发表时间:
1997-12
期刊:
British journal of rheumatology
影响因子:
--
通讯作者:
C. Baerwald;M. Laufenberg;T. Specht;P. Wichert;Gerd-Rüdiger Burmester;Andreas Krause
C. Baerwald;M. Laufenberg;T. Specht;P. Wichert;Gerd-Rüdiger Burmester;Andreas Krause
中科院分区:
其他
文献类型:
--
作者:
C. Baerwald;M. Laufenberg;T. Specht;P. Wichert;Gerd-Rüdiger Burmester;Andreas Krause

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以往的研究表明,免疫系统和自主神经系统之间的相互作用的改变可能有助于炎症性关节炎的发病机制。为了进一步解决这一问题,类风湿关节炎(RA)患者,本研究旨在确定β-肾上腺素能受体(β 2 R)对淋巴细胞亚群的调节及其对细胞反应性的影响。用免疫组化法检测RA患者和正常人外周血CD 4+、CD 8+淋巴细胞(PBL)和关节液淋巴细胞(SFL)β 2 R的表达。同时,研究了儿茶酚胺对OKT 3诱导的T细胞活化的影响。在RA患者中,与PBL上的β 2 R相比,SFL上的β 2 R显著降低。此外,观察到疾病活动相关的CD 8 + PBL上β 2 R显著降低。这种β 2 R的减少被降低的儿茶酚胺对OKT 3诱导的淋巴细胞增殖的抑制作用所抵消。我们的数据提供了进一步的证据,受损的交感神经对RA的免疫反应的影响。
Previous studies have demonstrated that an alteration of the interaction between the immune system and the autonomic nervous system may contribute to the pathogenesis of inflammatory arthritides. To address this issue further in patients with rheumatoid arthritis (RA), this study aimed at determining the modulation of beta-adrenergic receptors (beta 2R) on lymphocyte subsets and its impact on cell reactivity. beta 2R were determined on CD4+ and CD8+ peripheral blood lymphocytes (PBL) and synovial fluid lymphocytes (SFL) from RA patients and normal donors. In parallel, the influence of catecholamines on OKT3-induced T-cell activation was studied. In patients with RA, beta 2R on SFL were significantly decreased compared to beta 2R on PBL. Furthermore, a disease activity-correlated significant decrease of beta 2R on CD8+ PBL was observed. This decrease of beta 2R was paralleled by a reduced suppressive effect of catecholamines on OKT3-induced lymphocyte proliferation. Our data give further evidence for an impaired sympathetic influence on the immune response in RA.