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华勒氏变性可诱导大鼠大脑中Ia抗原的表达。

Wallerian degeneration induces Ia-antigen expression in the rat brain.

作者信息

Konno H, Yamamoto T, Iwasaki Y, Suzuki H, Saito T, Terunuma H

机构信息

Department of Neurological Sciences, Tohoku University School of Medicine, Sendai, Japan.

出版信息

J Neuroimmunol. 1989 Dec;25(2-3):151-9. doi: 10.1016/0165-5728(89)90132-x.

DOI:10.1016/0165-5728(89)90132-x
PMID:2685040
Abstract

Strong expression of class II major histocompatibility (MHC II, Ia) antigens was observed in areas of Wallerian degeneration following either a cryoinjury to the cerebral and cerebellar cortex or unilateral eye enucleation in adult Wistar and Lewis rats. The Wallerian degeneration was disclosed by the Fink-Heimer method but not by routine histological examination. The Ia antigens were localized exclusively to the cells labeled with OX-42 antibody and mistletoe-1 lectin (ML-1) and possessing the morphological identity of microglia. Development of Ia-expressing microglia at the sites of Wallerian degeneration was accompanied by neither tissue permeation of serum components as assessed by immunohistochemistry for autologous albumin nor tissue migration of hematogenous inflammatory cells.

摘要

在成年Wistar和Lewis大鼠中,对大脑和小脑皮质进行冷冻损伤或单侧眼球摘除后,在华勒氏变性区域观察到II类主要组织相容性(MHC II,Ia)抗原的强表达。华勒氏变性通过Fink-Heimer方法揭示,但常规组织学检查未发现。Ia抗原仅定位于用OX-42抗体和槲寄生-1凝集素(ML-1)标记且具有小胶质细胞形态特征的细胞。在华勒氏变性部位表达Ia的小胶质细胞的发育,既没有通过自体白蛋白免疫组织化学评估的血清成分组织渗透,也没有血源性炎症细胞的组织迁移。

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