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上皮内淋巴细胞表达的细胞毒性分子可能参与急性胃黏膜病变的发病机制。

Cytotoxic molecules expressed by intraepithelial lymphocytes may be involved in the pathogenesis of acute gastric mucosal lesions.

作者信息

Suzuki Takefumi, Ito Masafumi, Hayasaki Naoyuki, Ishihara Akira, Ando Takafumi, Ina Kenji, Kusugami Kazuo

机构信息

First Department of Internal Medicine, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.

出版信息

J Gastroenterol. 2003;38(3):216-21. doi: 10.1007/s005350300039.

Abstract

BACKGROUND

Little information is available on the precise mechanisms leading to the development of acute gastric mucosal lesions (AGMLs). We investigated whether the pathologic mechanism of AGMLs resulting in damage to epithelial cells is associated with cytotoxic molecules expressed by activated intraepithelial lymphocytes (IELs).

METHODS

The expression of the lymphocyte markers, CD3, CD4, CD8, CD20, T-cell-restricted intracellular antigen (TIA)-1, and granzyme B (GrB)-7 in IELs and that of single-stranded DNA (ssDNA) in apoptotic epithelial cells were evaluated by immunohistochemistry, using endoscopic biopsy specimens from 20 patients with AGMLs and 20 controls.

RESULTS

The number of CD3- and CD8-positive IELs increased in AGML specimens when compared with controls, and this increase was accompanied by a concomitant increase in TIA-1-positive cells. The epithelial cell layers of AGML specimens contained more GrB-7-positive phenotypically activated cytotoxic T cells than those in controls. Apoptotic ssDNA-positive epithelial cells were detected more frequently in AGML specimens than in controls, a feature which was paralleled by an increase in GrB-7-positive IELs in the former group of specimens.

CONCLUSIONS

The present study showed that activated cytotoxic IELs and apoptotic epithelial cells are increased in number in gastric mucosa affected with AGMLs. These results provide evidence that this condition could be categorized as apoptotic gastritis with activation of the innate immune response.

摘要

背景

关于导致急性胃黏膜病变(AGMLs)发生的确切机制,目前可用信息较少。我们研究了AGMLs导致上皮细胞损伤的病理机制是否与活化的上皮内淋巴细胞(IELs)表达的细胞毒性分子有关。

方法

使用20例AGMLs患者和20例对照的内镜活检标本,通过免疫组织化学评估IELs中淋巴细胞标志物CD3、CD4、CD8、CD20、T细胞限制性细胞内抗原(TIA)-1和颗粒酶B(GrB)-7的表达,以及凋亡上皮细胞中单链DNA(ssDNA)的表达。

结果

与对照相比,AGML标本中CD3和CD8阳性IELs的数量增加,并且这种增加伴随着TIA-1阳性细胞的相应增加。与对照相比,AGML标本的上皮细胞层含有更多GrB-7阳性的表型活化细胞毒性T细胞。AGML标本中检测到凋亡ssDNA阳性上皮细胞的频率高于对照,这一特征与前一组标本中GrB-7阳性IELs的增加平行。

结论

本研究表明,在受AGMLs影响的胃黏膜中,活化的细胞毒性IELs和凋亡上皮细胞的数量增加。这些结果提供了证据,表明这种情况可归类为伴有先天性免疫反应激活的凋亡性胃炎。

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