Nowaczyk M, Górski A, Korczak-Kowalska G, Wierzbicki P, Wyzgał J, Durlik M, Orłowska A
Department of Clinical Immunology, University Medical School, Warsaw, Poland.
Arch Immunol Ther Exp (Warsz). 1998;46(1):35-8.
Recent data indicate that extracellular matrix (ECM) proteins can provide costimulatory signals during the process of T cell activation. Those proteins accumulate in situ during allograft rejection; therefore, it may be expected that local ECM: T cell interactions may be relevant in the immunopathology of rejection. T cell adhesion from allograft of recipients with stable renal function (RAR-S) and patients with biopsy-proven chronic rejection (RAR-CH) to ECM proteins (collagen type IV, fibronectin, elastin) was measured. Furthermore, T cell: endothelial interactions in vitro were studied. Adhesion of PHA-activated T cells from both groups of allograft recipients to fibronectin, collagen type IV and elastin was significantly lower than in healthy blood donors. Moreover, similar pattern of activity was observed when T cell attachment to resting and activated endothelium was studied. There were no significant differences in the number of circulating CD45RO and CD4 positive T cells. We observed a higher (although not significantly) adhesion of the T cells to resting human dermal microvascular endothelial cells (HMEC) in the chronic stages of rejection, which can suggest that the immunosuppressive protocol used in the treatment of chronic rejection is insufficient to control immunopathologic phenomena occurring in that process. Therefore, it may be argued that too low immunosuppression can be one of the factors responsible for the development of this complication.
近期数据表明,细胞外基质(ECM)蛋白在T细胞活化过程中可提供共刺激信号。这些蛋白在同种异体移植排斥反应过程中于原位积聚;因此,可以预期局部ECM与T细胞的相互作用可能与排斥反应的免疫病理学相关。测定了肾功能稳定的移植受者(RAR-S)和经活检证实为慢性排斥反应的患者(RAR-CH)的同种异体移植T细胞对ECM蛋白(IV型胶原、纤连蛋白、弹性蛋白)的黏附情况。此外,还研究了体外T细胞与内皮细胞的相互作用。两组移植受者中经PHA激活的T细胞对纤连蛋白、IV型胶原和弹性蛋白的黏附力均显著低于健康献血者。此外,在研究T细胞与静息及活化内皮细胞的附着情况时,观察到了类似的活性模式。循环中的CD45RO和CD4阳性T细胞数量没有显著差异。我们观察到在排斥反应的慢性阶段,T细胞对静息人真皮微血管内皮细胞(HMEC)的黏附力更高(尽管不显著),这可能表明用于治疗慢性排斥反应的免疫抑制方案不足以控制该过程中发生的免疫病理现象。因此,可以认为免疫抑制过低可能是导致这种并发症发生的因素之一。