Wahle M, Pierer M, Krause A, Kolker S, Baerwald C G O
University Hospital Leipzig, Department of Medicine IV, Leipzig, Germany.
Ann N Y Acad Sci. 2002 Jun;966:425-8. doi: 10.1111/j.1749-6632.2002.tb04243.x.
The expression of beta2-adrenergic receptors (beta2-R) on B lymphocytes and agonist-induced cAMP production is reduced in patients with rheumatoid arthritis (RA). To further study functional consequences of the diminished beta2-R density on B lymphocytes in RA patients, agonist-induced cell death was evaluated and compared to healthy controls. B lymphocytes from patients with RA and healthy controls were activated with anti-IgM-antibody. Coincubation was carried out with isoprenaline (iso, 0.001-10 microM). Apoptotic and necrotic cells were determined using Annexin-V and propidium-iodide staining. beta2-R-induced cell death in B cells from healthy volunteers was stimulated after 24 h (medium, 21.2 +/- 1.6%; iso, 34.6 +/- 4.4%; increase 59.3 +/- 10.1%). However, in RA patients the increase in cell death following beta2-R stimulation (21.8 +/- 8.9%) was significantly impaired (p = 0.02). Our data demonstrate that catecholamine-induced cell death after stimulation of beta2-R on B lymphocytes is decreased in RA patients, possibly contributing to the pathogenesis of the disease.
类风湿关节炎(RA)患者B淋巴细胞上β2-肾上腺素能受体(β2-R)的表达及激动剂诱导的环磷酸腺苷(cAMP)生成均减少。为进一步研究RA患者B淋巴细胞上β2-R密度降低的功能后果,对激动剂诱导的细胞死亡进行了评估,并与健康对照者进行比较。用抗IgM抗体激活RA患者和健康对照者的B淋巴细胞。与异丙肾上腺素(异,0.001 - 10微摩尔)共同孵育。使用膜联蛋白V和碘化丙啶染色测定凋亡细胞和坏死细胞。24小时后,健康志愿者B细胞中β2-R诱导的细胞死亡受到刺激(培养基,21.2±1.6%;异,34.6±4.4%;增加59.3±10.1%)。然而,在RA患者中,β2-R刺激后细胞死亡的增加(21.8±8.9%)明显受损(p = 0.02)。我们的数据表明,RA患者中B淋巴细胞上β2-R刺激后儿茶酚胺诱导的细胞死亡减少,这可能与该疾病的发病机制有关。