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小鼠基因型对免疫复合物介导的被动全身过敏反应的影响。

Influence of mouse genotype on passive systemic anaphylaxis by immune complexes.

作者信息

Portolés A, Rojo J M, Díaz R

出版信息

Infect Immun. 1986 Dec;54(3):882-5. doi: 10.1128/iai.54.3.882-885.1986.

Abstract

The influence of mouse genotype on passive systemic anaphylaxis (PSA) by immune complexes was studied. PSA was induced by using Brucella abortus endotoxin as the antigen and rabbit anti-Brucella endotoxin antisera. Experiments using syngeneic mice as well as mice congenic for H-2 showed that the H-2 haplotype influenced the sensitivity of mice to PSA. Among the H-2 haplotypes studied, H-2b was the most sensitive, followed by H-2k and H-2d. Experiments using passive transfer of serum as well as the complement inhibitors suramin and flufenamic acid indicated that variations in complement levels under control of H-2 may be responsible for the effects described. Cyproheptadine, a blocker of serotonin and histamine receptors, and imidazol-alpha-ketoglutarate, an inhibitor of thromboxane synthesis, inhibited PSA, indicating that platelet aggregation, possibly mediated by activated components of the complement cascade, is an important feature in the development of PSA reactions in this system. Differences between strains for protection by cyproheptadine and for the effect of complement inhibitors indicated a role of early components of the classical pathway in this model.

摘要

研究了小鼠基因型对免疫复合物介导的被动全身过敏反应(PSA)的影响。以流产布鲁氏菌内毒素作为抗原,兔抗布鲁氏菌内毒素抗血清诱导产生PSA。使用同基因小鼠以及H-2基因座同源的小鼠进行的实验表明,H-2单倍型影响小鼠对PSA的敏感性。在所研究的H-2单倍型中,H-2b最敏感,其次是H-2k和H-2d。使用血清被动转移以及补体抑制剂苏拉明和氟芬那酸进行的实验表明,在H-2控制下补体水平的变化可能是上述效应的原因。血清素和组胺受体阻滞剂赛庚啶以及血栓素合成抑制剂咪唑-α-酮戊二酸可抑制PSA,这表明可能由补体级联激活成分介导的血小板聚集是该系统中PSA反应发生的一个重要特征。赛庚啶的保护作用以及补体抑制剂的效应在不同品系之间存在差异,这表明经典途径的早期成分在该模型中起作用。

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1
BOUND COMPLEMENT AND IMMUNOLOGIC INJURY OF BLOOD VESSELS.补体结合与血管的免疫损伤
J Exp Med. 1965 Feb 1;121(2):215-34. doi: 10.1084/jem.121.2.215.
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Protective effects of thromboxane A2 synthetase inhibitors on endotoxin shock.
Prostaglandins Leukot Med. 1983 Jun;11(2):179-88. doi: 10.1016/0262-1746(83)90018-5.
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The role of complement in experimental disease models.补体在实验性疾病模型中的作用。
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