Soluble Fc gamma RIIIa is present in plasma and is derived from natural killer cells.
Soluble Fc gamma RIIIa is present in plasma and is derived from natural killer cells.
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可溶性 Fc gamma RIIIa 存在于血浆中，源自自然杀伤细胞。
DOI：
10.4049/jimmunol.152.2.900
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发表时间：
1994
影响因子：
4.4
通讯作者：
A. von dem Borne
中科院分区：
文献类型：
--
作者：
M. de Haas;M. Kleijer;R. Minchinton;D. Roos;A. von dem Borne
Fc γ RIII（CD 16）是复合IgG的一种受体，由两种非常同源的基因编码：Fc γ RIIIA和Fc γ RIIIB。NK细胞和巨噬细胞表达Fe γ RIIla，而只有中性粒细胞组成性表达Fe γ RIIlb。在先前的研究中，我们发现血浆中的可溶性Fc γ RIII似乎仅来源于中性粒细胞。然而，针对Fc γ RIII不同表位的CD 16 mAb从纯合Fc γ RIIIB基因缺陷供体的血浆中沉淀糖蛋白。该糖蛋白以与释放的源自NK细胞的Fc γ RIIIa相似的方式迁移，而由培养的单核细胞释放的Fc γ RIIIa迁移不同，并且在SDS-PAGE上似乎更严重地糖基化。去糖基化后，血浆sFc γ RIIIa的M（r）与释放的Fc γ RIIIa相似。此外，V8蛋白酶图谱是相同的。因此，我们得出结论，sFc γ RIIIa也存在于血浆中，并且来源于NK细胞。由于在大多数纯合Fc γ RIIIB基因缺陷供体的血浆中几乎检测不到sFc γ RIII水平，因此我们怀疑与健康供体血浆中的sFc γ RIIIb水平相比，sFc γ RIIIa水平可忽略不计。2例NK细胞淋巴细胞增多症患者的sFc γ RIIIaNK血浆水平较高。此外，在两名类风湿性关节炎患者的血浆中发现高水平的sFc γ RIIIaNK。因此，sFc γ RIIIaNK的水平可能反映了某些疾病中循环NK细胞的增加或Fc γ RIIIaNK的释放增强。这项研究表明，区分sFc gamma RIIla和sFc gamma RIIIb的测定对于解释患者的sFc gamma RIII水平是必要的。
Fc gamma RIII (CD16), a receptor for complexed IgG, is encoded by two very homologous genes: Fc gamma RIIIA and Fc gamma RIIIB. NK cells and macrophages express Fc gamma RIIIa, whereas only neutrophils constitutively express Fc gamma RIIIb. In a previous study we found that soluble (s)Fc gamma RIII in plasma seemed to originate only from neutrophils. However, CD16 mAb, directed against different epitopes of Fc gamma RIII, precipitated a glycoprotein from plasma of homozygous Fc gamma RIIIB gene-deficient donors. This glycoprotein migrated in a similar way as did released Fc gamma RIIIa derived from NK cells, whereas Fc gamma RIIIa released by cultured monocytes migrated differently and appeared to be more heavily glycosylated on SDS-PAGE. After deglycosylation, the M(r) of the plasma sFc gamma RIIIa was similar to that of released Fc gamma RIIIa. Moreover, V8-protease maps were identical. Therefore, we conclude that sFc gamma RIIIa is also present in plasma and is derived from NK cells. Because sFc gamma RIII levels are hardly detectable in the plasma of most homozygous Fc gamma RIIIB gene-deficient donors, we suspect that the sFc gamma RIIIa level is negligible compared with the level of sFc gamma RIIIb in plasma of healthy donors. Two patients with an NK cell lymphocytosis had a high plasma level of sFc gamma RIIIaNK. Furthermore, high levels of sFc gamma RIIIaNK were found in plasma of two patients with rheumatoid arthritis. Thus, the level of sFc gamma RIIIaNK might reflect either an increase in circulating NK cells or an enhanced release of Fc gamma RIIIaNK in certain diseases. This study shows that an assay that discriminates between sFc gamma RIIIa and sFc gamma RIIIb is necessary for the interpretation of sFc gamma RIII levels in patients.