NA‐phenotype‐dependent differences in neutrophil FcγRIIIb expression cause differences in plasma levels of soluble FcγRIII
NA‐phenotype‐dependent differences in neutrophil FcγRIIIb expression cause differences in plasma levels of soluble FcγRIII
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中性粒细胞 FcγRIIIb 表达的 NA 表型依赖性差异导致可溶性 FcγRIII 血浆水平的差异
DOI：
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发表时间：
1996
期刊：
影响因子：
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通讯作者：
A. von dem Borne
中科院分区：
文献类型：
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作者：
H. Koene;M. Haas;M. Kleijer;D. Roos;A. von dem Borne
血浆中的可溶性FcγRIII主要来源于中性粒细胞，是全身中性粒细胞质量的指标。我们已经开发了一种新的、灵敏的“夹心”ELISA来测量血浆中可溶性FcγRIII和细胞上清液中释放的FcγRIII。在试验中可检出来源于NK细胞的sFcγRIIIa和来源于中性粒细胞的sFcγRIIIb。然而，FcγRIIIB基因缺陷供体的血浆分析表明，sFcγRIIIa仅对健康个体中测得的总量有轻微贡献。此外，我们观察到纯合NA1阳性供体血浆中sFcγRIII含量低于纯合NA2阳性供体血浆。发现杂合子供体血浆中sFcγRIII水平中等。发现半合子FcγRIIIB基因缺陷供体血浆中sFcγRIII的量是具有两个FcγRIIIB等位基因的供体的一半。血浆sFcγRIII中的这些NA表型依赖性差异不能归因于中性粒细胞活化后FcγRIIIb脱落的试验假象或NA依赖性差异。用纯合供体血浆构建的校准曲线未显示抗体亲和力的NA依赖性差异。测量PMA刺激的中性粒细胞上清液中释放的FcγRIIIb，以及用人IgG抑制该信号，结果显示无NA依赖性差异。然而，中性粒细胞FcγRIIIb表达存在NA依赖性差异，与sFcγRIII血浆水平的差异相当。NA型凋亡中性粒细胞上清液中释放的FcγRIII量的差异与FcγRIIIb表达的初始差异相似，NA 1阳性供体中的Fc γRIIIb表达也低于杂合子和NA 2阳性供体。总之，可溶性FcγRIII血浆水平的NA依赖性差异似乎是由中性粒细胞膜上受体表达的差异引起的。
Soluble FcγRIII in plasma is primarily derived from neutrophils and is a measure of the total body neutrophil mass. We have developed a new, sensitive ‘sandwich’ ELISA to measure soluble FcγRIII in plasma and released FcγRIII in cell supernatants. Both sFcγRIIIa, derived from NK cells and sFcγRIIIb, derived from neutrophils are detected in the assay. However, plasma analysis of FcγRIIIB gene‐deficient donors suggested that sFcγRIIIa contributes only marginally to the total amount measured in healthy individuals. Furthermore, we observed that plasma of homozygous NA1‐positive donors contained lower amounts of sFcγRIII than plasma of homozygous NA2‐positive donors. Heterozygous donors were found to have intermediate levels of sFcγRIII in their plasma. Hemizygous FcγRIIIB gene‐deficient donors were found to have half the amount of sFcγRIII in their plasma compared to donors with two FcγRIIIB alleles. These NA phenotype‐dependent differences in plasma sFcγRIII could not be contributed to either an assay artefact or NA‐dependent differences in shedding of FcγRIIIb upon neutrophil activation. Calibration curves constructed with plasma of homozygous donors did not reveal NA‐dependent differences in antibody affinity. Measurement of released FcγRIIIb in supernatants of neutrophils stimulated with PMA, and inhibition of this signal with human IgG revealed no NA‐dependent differences. However, NA‐dependent differences in neutrophil FcγRIIIb expression were present, comparable to the differences found in plasma levels of sFcγRIII. Differences in the amounts of released FcγRIII in supernatants of NA‐typed apoptotic neutrophils were similar to initial differences in FcγRIIIb expression, again being lower in NA1‐positive than in heterozygous and NA2‐positive donors. In conclusion, NA‐dependent differences in plasma levels of soluble FcγRIII seem to be caused by differences in expression of the receptor on the neutrophil membrane.
影响因子：
20.3
作者：
H. Fleit;C. Kobasiuk;C. Daly;R. Furie;PC Levy;RO Webster
通讯作者：
H. Fleit;C. Kobasiuk;C. Daly;R. Furie;PC Levy;RO Webster