Increased expression of an adhesion-promoting surface glycoprotein in the granulocytopenia of hemodialysis.
Increased expression of an adhesion-promoting surface glycoprotein in the granulocytopenia of hemodialysis.
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血液透析粒细胞减少症中促粘附表面糖蛋白的表达增加。
DOI：
10.1056/nejm198502213120801
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Colten,HR
中科院分区：
文献类型：
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作者：
Arnaout,MA;Hakim,RM;Todd3rd,RF;Dana,N;Colten,HR
为了确定血液透析引起粒细胞减少的机制，我们进行了粒细胞黏附促进表面糖蛋白(MO1)的定量动力学研究。在8名接受维持性血液透析的患者中，在使用新的铜丙烷膜开始透析后15分钟内，MO1的平均细胞表面表达增加了5倍。表面MO1的峰值增加与中性粒细胞计数的最大下降和补体激活产物C5a desArg和C3a desArg水平的峰值上升相一致。在第五次重复使用的膜上进行透析时，没有发现明显的补体激活，没有发现MO1表达增加，中性粒细胞计数也没有变化。C5a desArg(但不是C3a desArg)在体外以与体内测量相似的浓度诱导正常粒细胞上MO1的表达增加。趋化性多肽诱导的粒细胞聚集(细胞间黏附增加的反映)在体外可被小鼠抗MO1的单抗特异性阻断。这些数据表明，体内粒细胞上MO1表达的增加部分是由C5a(和C5a desArg)介导的。在血液透析过程中，粒细胞表面MO1的数量增加可能提供了一种启动白细胞聚集、粒细胞隔离和中性粒细胞减少的机制。《英国医学杂志》1985；312：457-62。
To identify the mechanisms accounting for hemodialysis-induced granulocytopenia, we undertook quantitative kinetic studies of a granulocyte-adhesion–promoting surface glycoprotein (Mo1).In eight patients undergoing maintenance hemodialysis, there was a fivefold increase in the mean cell-surface expression of Mo1 within 15 minutes after the start of dialysis with a new cuprophane membrane. The peak increase in surface Mo1 coincided with the maximal drop in neutrophil count and with the peak rise in the plasma levels of the complement-activation products C5a desArg and C3a desArg. During dialysis on a membrane being reused for the fifth time, no significant complement activation, no increase in Mo1 expression, and no change in neutrophil count were seen. C5a desArg (but not C3a desArg) induced a comparable increase in Mo1 expression on normal granulocytes in vitro at concentrations similar to those measured in vivo. Chemotactic peptide–induced granulocyte aggregation (a reflection of increased cell-to-cell adhesiveness) was specifically blocked by mouse monoclonal antibodies to Mo1 in vitro.These data suggest that the increased expression of Mo1 on granulocytes in vivo is in part mediated by C5a (and C5a desArg). The quantitative increase in granulocyte-surface Mo1 may provide a mechanism for initiating leukoaggregation, sequestration of granulocytes, and neutropenia during hemodialysis. (N Engl J Med 1985; 312:457–62.)