Plesner T, Karle H, Rubin B, Thomsen M
Clin Exp Immunol. 1978 Feb;31(2):269-75.
Cell-associated and serum beta2-microglobulin was estimated in seven patients with chronic lymphocytic leukaemia. The amount of cell-associated beta2-microglobulin was significantly reduced (P less than 0.01), due to a decrease in the fraction of beta2-microglobulin that passes unretarded through a concanavalin A affinity column (presumably non-HLA-associated beta2-microglobulin). Serum concentrations of beta2-microglobulin were increased, but no correlation was found between the decrease in cell-associated beta2-microglobulin and the increase in serum beta2-microglobulin. All of the beta2-microglobulin from leukaemic serum was eluted corresponding to a molecular weight of 11,800 and none of it was retarded on a concanavalin A affinity column. The decrease in cell-associated beta2-microglobulin might reflect a change in the qualitative or quantitative expression of beta2-microglobulin-associated membrane structures on the leukaemic cells, perhaps conferring resistance to the cells against hypothetical immunological host defence mechanisms.
对7例慢性淋巴细胞白血病患者的细胞相关β2-微球蛋白和血清β2-微球蛋白进行了评估。细胞相关β2-微球蛋白的量显著降低(P<0.01),这是由于通过伴刀豆球蛋白A亲和柱未被阻滞的β2-微球蛋白部分(推测为非HLA相关的β2-微球蛋白)减少所致。血清β2-微球蛋白浓度升高,但细胞相关β2-微球蛋白的降低与血清β2-微球蛋白的升高之间未发现相关性。白血病血清中的所有β2-微球蛋白均以分子量11,800被洗脱,且在伴刀豆球蛋白A亲和柱上均未被阻滞。细胞相关β2-微球蛋白的降低可能反映了白血病细胞上β2-微球蛋白相关膜结构在定性或定量表达上的变化,这或许赋予了细胞对假设的免疫宿主防御机制的抗性