Botto M, So A K, Giles C M, Mason P D, Walport M J
Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London.
Br J Haematol. 1990 May;75(1):106-11. doi: 10.1111/j.1365-2141.1990.tb02624.x.
It has previously been shown, by a haemagglutination assay, that patients with systemic lupus erythematosus (SLE) express increased levels of HLA class I on erythrocytes compared with normal subjects and patients with rheumatoid arthritis (RA). A radioligand-binding assay, using monoclonal antibody W6/32, was devised to quantify HLA class I expression on erythrocytes and platelets. An increased number of class I molecules was expressed on erythrocytes from 45 patients with SLE (mean = 354 molecules per cell, median = 255 molecules, range = 30-1270 molecules per cell), compared with cells from 46 normal subjects (mean = 132, median = 78, range = 40-550) and 31 RA patients (mean = 132, median = 89, range = 26-497). The presence of HLA-B7 correlated with increased class I expression on erythrocytes from both normal subjects and patients with SLE. Levels of HLA class I in serum were measured. All subjects with HLA-A9 (A23, 24) showed higher levels of serum class I than their A9-negative counterparts, and there was no difference in levels between SLE patients and normal subjects. There were no correlations between class I levels in serum and on erythrocytes amongst SLE patients or normal subjects. Red cells were fractionated, according to their age in vivo, on Percoll gradients. Class I levels fell with increasing erythrocyte age in all individuals, but were higher in all fractions from SLE patients compared with age-matched fractions from normal subjects. HLA-B7-positive erythrocytes also expressed higher class I levels in each Percoll fraction, compared with their HLA-B7-negative counterparts, suggesting that enhanced B7 expression is not due to greater structural stability of this class I allotype. These data are compatible with the hypothesis that class I is expressed as an intrinsic protein of erythrocyte membranes and that expression is increased amongst patients with SLE.
此前通过血细胞凝集试验已表明，与正常受试者及类风湿关节炎（RA）患者相比，系统性红斑狼疮（SLE）患者红细胞上的HLA I类分子表达水平升高。设计了一种使用单克隆抗体W6/32的放射性配体结合试验，以定量红细胞和血小板上的HLA I类分子表达。45例SLE患者红细胞上表达的I类分子数量增加（平均每个细胞354个分子，中位数255个分子，范围为每个细胞30 - 1270个分子），相比之下，46例正常受试者的细胞（平均132个，中位数78个，范围40 - 550个）和31例RA患者的细胞（平均132个，中位数89个，范围26 - 497个）。HLA - B7的存在与正常受试者及SLE患者红细胞上I类分子表达增加相关。检测了血清中HLA I类分子水平。所有携带HLA - A9（A23、24）的受试者血清I类分子水平均高于其A9阴性的对应者，且SLE患者与正常受试者之间的水平无差异。SLE患者或正常受试者血清和红细胞上的I类分子水平之间无相关性。根据红细胞在体内的年龄，在Percoll梯度上对红细胞进行分级分离。在所有个体中，I类分子水平随红细胞年龄增加而下降，但与年龄匹配的正常受试者分级相比，SLE患者所有分级中的I类分子水平更高。与HLA - B7阴性的对应红细胞相比，HLA - B7阳性红细胞在每个Percoll分级中也表达更高的I类分子水平，这表明B7表达增强并非由于该I类同种异型的结构稳定性更高。这些数据与以下假设相符：I类分子作为红细胞膜的内在蛋白表达，且在SLE患者中表达增加。
