Currie M S, Weinberg J B, Rustagi P K, Logue G L
Blood. 1987 Feb;69(2):529-36.
Patients with syndromes of autoantibody-mediated hematocytopenias may manifest signs of increased cell destruction and/or decreased cell production, depending on the maturity of the target cell and the effects of antibody binding. The purpose of this study was to use a cultured human cell line of hematopoietic origin for in vitro assays of antibody binding to overcome the relative inaccessibility of natural human marrow progenitor cells. This report describes the detection, using radioiodinated staphylococcal protein A (SPA), of antibodies binding to a human promyelocytic cell line (HL-60) in sera from three patients with chronic idiopathic granulocytic hypoplasia ("pure white cell aplasia," PWCA) and 22 patients with other syndromes of suspected immune neutropenia. Bone marrow from patients with increased IgG binding to HL-60 cells showed less than 15% granulocytic lineage cellularity in 11 of 17 cases. In vitro differentiation of HL-60 cells by retinoic acid resulted in increased IgG binding for sera that had shown increased IgG binding to mature granulocytes but not undifferentiated HL-60 cells; in contrast, for sera with antibodies to untreated HL-60 cells and for normal serum, in vitro differentiation had little effect on IgG binding. Antibodies eluted from mature granulocytes were similar to the parent serum regarding the ratio of IgG binding to mature cells v HL-60 cells. No sera from 19 patients with febrile transfusion reactions showed increased IgG binding to HL-60 cells in the absence of increased IgG binding to mature granulocytes, although two sera had antibodies to both cell types. The use of HL-60 cells as targets may permit measurement of serum antibodies associated with granulocytic hypoplasia. In combination with assays to detect antibody binding to mature granulocytes, these techniques may discriminate among autoantibody specificities for antigens that are gained, conserved, or lost during myeloid maturation.
自身抗体介导的血细胞减少综合征患者可能表现出细胞破坏增加和/或细胞生成减少的迹象，这取决于靶细胞的成熟度以及抗体结合的影响。本研究的目的是使用一种造血来源的培养人细胞系进行抗体结合的体外测定，以克服天然人骨髓祖细胞相对难以获取的问题。本报告描述了使用放射性碘化葡萄球菌蛋白A（SPA）检测三例慢性特发性粒细胞发育不全（“纯白细胞再生障碍”，PWCA）患者和22例疑似免疫性中性粒细胞减少症其他综合征患者血清中与人类早幼粒细胞系（HL-60）结合的抗体。在17例中有11例，与HL-60细胞IgG结合增加的患者骨髓中粒细胞系细胞比例低于15%。维甲酸对HL-60细胞进行体外分化后，对于那些与成熟粒细胞IgG结合增加但与未分化HL-60细胞IgG结合未增加的血清，其IgG结合增加；相反，对于含有针对未处理HL-60细胞抗体的血清和正常血清，体外分化对IgG结合影响很小。从成熟粒细胞洗脱的抗体与母血清在与成熟细胞和HL-60细胞的IgG结合比例方面相似。19例发热性输血反应患者的血清中，在与成熟粒细胞IgG结合未增加的情况下，未显示与HL-60细胞IgG结合增加，尽管有两份血清对两种细胞类型均有抗体。使用HL-60细胞作为靶标可能有助于检测与粒细胞发育不全相关的血清抗体。结合检测抗体与成熟粒细胞结合的测定，这些技术可能区分自身抗体对髓系成熟过程中获得、保留或丢失的抗原的特异性。
