Wilbrink B, Bijlsma J W, Huber-Bruning O, Van Roy J L, Den Otter W, Van Eden W
Department of Rheumatology, University Hospital Utrecht, The Netherlands.
J Rheumatol. 1990 Apr;17(4):532-7.
In a coculture with porcine articular cartilage explants unstimulated blood mononuclear cells (BMC) from patients with rheumatoid arthritis (RA), but not from healthy controls, induced proteoglycan depletion of dead cartilage. Specific stimulation of the RA BMC with Mycobacterium tuberculosis (MT), in comparison with concanavalin A (Con-A), strongly enhanced the proteoglycan depletion of living cartilage; this was not found with the BMC of healthy controls. However, the MT induced proliferative responses of the same BMC were similar in healthy controls and patients with RA. Neither the proliferative response nor the proteoglycan depletion was influenced by the presence of HLA-DR4 in the donor, whether patients with RA or healthy control. The proliferative responses of the RA BMC seemed to correlate inversely with the proteoglycan depletion. We conclude that stimulation of RA BMC with mycobacterial antigens may elicit effector pathways that induce proteoglycan depletion, independent of T cell proliferation.
在与猪关节软骨外植体的共培养中，类风湿关节炎（RA）患者未受刺激的血液单核细胞（BMC）可导致死亡软骨的蛋白聚糖耗竭，而健康对照者的则不会。与伴刀豆球蛋白A（Con - A）相比，用结核分枝杆菌（MT）特异性刺激RA - BMC可强烈增强活软骨的蛋白聚糖耗竭；健康对照者的BMC未出现这种情况。然而，MT诱导的相同BMC的增殖反应在健康对照者和RA患者中相似。供体中是否存在HLA - DR4，无论是RA患者还是健康对照者，都不会影响增殖反应和蛋白聚糖耗竭。RA - BMC的增殖反应似乎与蛋白聚糖耗竭呈负相关。我们得出结论，用分枝杆菌抗原刺激RA - BMC可能引发诱导蛋白聚糖耗竭的效应途径，而与T细胞增殖无关。
