Cohen J H, Lutz H U, Pennaforte J L, Bouchard A, Kazatchkine M D
Laboratoire d'Immunologie, CHU Robert Debré, Reims, France.
Clin Exp Immunol. 1992 Mar;87(3):422-8. doi: 10.1111/j.1365-2249.1992.tb03013.x.
The present study investigated the rate of catabolism of CR1 (the C3b receptor, CD35) on erythrocytes (E) in vivo, in relationship with the expressed number of CR1/E, the CR1.1 HindIII quantitative CR1 polymorphism, and cell age. The relationship between the number of CR1/E and cell age was analysed by measuring G6PDH activity in E that had been sorted according to high or low expression of CR1 (CD35), by assessing the expression of CR1 (CD35) on E separated according to cell density, and by comparing the number of CR1 (CD35) antigenic sites on reticulocytes and on E. A physiological catabolism of CR1 (CD35) manifested by a reduction in the number of CR1 (CD35) antigenic sites/E with cell ageing was consistently observed in healthy individuals. The number of CR1/E decreased with ageing of E according to a complex pattern that associated an exponential decay and an offset. Calculated half-lives of CR1 (CD35) ranged between 11 and 32 days in healthy individuals. A more rapid loss of CR1 (CD35) with cell ageing occurred on cells from individuals expressing high numbers of CR1/E. In patients with systemic lupus erythematosus (SLE), half-lives of CR1 (CD35) on E were in the same range as those of healthy individuals with a similar quantitative CR1 genotype; the number of CR1 (CD35) on reticulocytes was reduced and linearly related to the number of CR1/E, independently of the patients' quantitative CR1 genotype. Transfusion experiments with E bearing high or low amounts of CR1/E indicated the lack of preferential removal of E bearing high numbers of CR1 (CD35) in patients with SLE. These results indicate that the rate of loss of CR1 (CD35) from E with cell ageing is directly related to the quantitative CR1 phenotype and suggest that enhanced peripheral catabolism is not the sole mechanism of the acquired loss of CR1 (CD35) on E in patients with SLE.
本研究调查了体内红细胞（E）上CR1（C3b受体，CD35）的分解代谢率，及其与CR1/E的表达数量、CR1.1 HindIII定量CR1多态性和细胞年龄的关系。通过测量根据CR1（CD35）高表达或低表达分选的E中的G6PDH活性，评估根据细胞密度分离的E上CR1（CD35）的表达，并比较网织红细胞和E上CR1（CD35）抗原位点的数量，分析了CR1/E数量与细胞年龄之间的关系。在健康个体中持续观察到，随着细胞衰老，CR1（CD35）抗原位点/E数量减少，这表明CR1（CD35）存在生理性分解代谢。CR1/E的数量随着E的衰老而减少，呈现出指数衰减和偏移相关的复杂模式。健康个体中CR1（CD35）的计算半衰期在11至32天之间。在表达大量CR1/E的个体的细胞上，随着细胞衰老，CR1（CD35）的丢失更快。在系统性红斑狼疮（SLE）患者中，E上CR1（CD35）的半衰期与具有相似定量CR1基因型的健康个体相同；网织红细胞上CR1（CD35）的数量减少，且与CR1/E的数量呈线性相关，与患者的定量CR1基因型无关。对携带大量或少量CR1/E的E进行输血实验表明，SLE患者中不存在优先清除携带大量CR1（CD35）的E的情况。这些结果表明，随着细胞衰老，E上CR1（CD35）的丢失率与定量CR1表型直接相关，并表明增强的外周分解代谢不是SLE患者E上CR1（CD35）获得性丢失的唯一机制。
