Inhibition of autoantibody binding to platelet glycoprotein IIb/IIIa by anti-idiotypic antibodies in intravenous gammaglobulin
Inhibition of autoantibody binding to platelet glycoprotein IIb/IIIa by anti-idiotypic antibodies in intravenous gammaglobulin
复制标题
静脉注射丙种球蛋白中抗独特型抗体抑制自身抗体与血小板糖蛋白 IIb/IIIa 的结合
DOI:
10.1182/blood.v74.7.2414.bloodjournal7472414
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发表时间:
1989
期刊:
影响因子:
20.3
通讯作者:
R. Mcmillan
中科院分区:
文献类型:
--
作者:
P. Berchtold;G. Dale;P. Tani;R. Mcmillan
Intravenous immunoglobulin (IVIgG) causes an acute rise in the platelet count in the majority of patients with chronic immune thrombocytopenic purpura (ITP) but the mechanism(s) of action is still unknown. We evaluated the ability of three different IVIgG preparations to inhibit the in vitro binding of autoantibody to platelet glycoprotein (GP) IIb/IIIa. ITP plasma, known to contain anti-GPIIb/IIIa antibodies, was incubated overnight with either IVIgG or bovine serum albumin (BSA) followed by measurement of the autoantibody titer. Binding of autoantibody from eight ITP patients was inhibited by IVIgG in proportion to the IVIgG concentration. Using 3.2% IVIgG, compatible with therapeutic concentrations expected in vivo, mean inhibition of autoantibody binding ranged from 20.2% to 41.3%. No inhibition by IVIgG of alloantibody binding to the same or different molecules was detected (five patients with anti-GPIIb/IIIa and two with anti-HLA alloantibodies). F(ab')2 fragments of IVIgG also inhibited the binding of both plasma autoantibodies and purified anti-GPIIb/IIIA autoantibodies prepared by elution from antigen affinity columns. A portion of the anti-idiotypic antibodies could be adsorbed from IVIgG using insolubilized, purified anti-GPIIb/IIIa autoantibody. These results show that IVIgG preparations from normal donors contain anti-idiotypic antibodies directed against idiotypes located on GPIIb/IIIa autoantibodies but do not have anti-idiotypes to platelet alloantibodies against the same or different molecules. The importance of these anti-idiotypic antibodies in the therapeutic response to IVIgG remains to be established.
影响因子:
20.3
作者:
R. Mcmillan;P. Tani;F. Millard;P. Berchtold;Renshaw Lw;V. Woods
通讯作者:
R. Mcmillan;P. Tani;F. Millard;P. Berchtold;Renshaw Lw;V. Woods
DOI:
--
发表时间:
1988
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Ward,RE;McNamara-Ward,M;Webb,CF;Altman,D;Lim,PL;Tucker,PW;Kohler,H
通讯作者:
Kohler,H