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本文引用的文献

1
The effect of class II major histocompatibility complex expression on adherence of Helicobacter pylori and induction of apoptosis in gastric epithelial cells: a mechanism for T helper cell type 1-mediated damage.II类主要组织相容性复合体表达对幽门螺杆菌黏附及胃上皮细胞凋亡诱导的影响:1型辅助性T细胞介导损伤的一种机制
J Exp Med. 1998 May 18;187(10):1659-69. doi: 10.1084/jem.187.10.1659.
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Lymphocytes in the human gastric mucosa during Helicobacter pylori have a T helper cell 1 phenotype.幽门螺杆菌感染时,人胃黏膜中的淋巴细胞具有辅助性T细胞1表型。
Gastroenterology. 1998 Mar;114(3):482-92. doi: 10.1016/s0016-5085(98)70531-1.
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Antigastric autoantibodies in Helicobacter pylori infection: implications of histological and clinical parameters of gastritis.幽门螺杆菌感染中的抗胃自身抗体:胃炎组织学和临床参数的意义
Gut. 1997 Nov;41(5):619-23. doi: 10.1136/gut.41.5.619.
4
Murine CD4 T-cell response to Helicobacter infection: TH1 cells enhance gastritis and TH2 cells reduce bacterial load.小鼠CD4 T细胞对幽门螺杆菌感染的反应:TH1细胞加剧胃炎,而TH2细胞降低细菌载量。
Gastroenterology. 1997 Dec;113(6):1848-57. doi: 10.1016/s0016-5085(97)70004-0.
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Differential stimulation of interleukin-12 (IL-12) and IL-10 by live and killed Helicobacter pylori in vitro and association of IL-12 production with gamma interferon-producing T cells in the human gastric mucosa.活的和灭活的幽门螺杆菌在体外对白细胞介素-12(IL-12)和IL-10的差异刺激以及人胃黏膜中IL-12产生与产生γ干扰素的T细胞的关联
Infect Immun. 1997 Oct;65(10):4229-35. doi: 10.1128/iai.65.10.4229-4235.1997.
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Different cytokine profile and antigen-specificity repertoire in Helicobacter pylori-specific T cell clones from the antrum of chronic gastritis patients with or without peptic ulcer.患有或不患有消化性溃疡的慢性胃炎患者胃窦部幽门螺杆菌特异性T细胞克隆中不同的细胞因子谱和抗原特异性库。
Eur J Immunol. 1997 Jul;27(7):1751-5. doi: 10.1002/eji.1830270723.
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Molecular mimicry between Helicobacter pylori and the host.幽门螺杆菌与宿主之间的分子模拟
Trends Microbiol. 1997 Feb;5(2):70-3. doi: 10.1016/S0966-842X(96)10084-6.
8
Expression of mRNA for interferon-gamma, interleukin-10, and interleukin-12 (p40) in normal gastric mucosa and in mucosa infected with Helicobacter pylori.正常胃黏膜及幽门螺杆菌感染黏膜中γ-干扰素、白细胞介素-10和白细胞介素-12(p40)的mRNA表达
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9
T helper 1 effector cells specific for Helicobacter pylori in the gastric antrum of patients with peptic ulcer disease.消化性溃疡病患者胃窦中针对幽门螺杆菌的辅助性T1效应细胞。
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10
Antigenic mimicry between Helicobacter pylori and gastric mucosa in the pathogenesis of body atrophic gastritis.幽门螺杆菌与胃黏膜之间的抗原模拟在胃体萎缩性胃炎发病机制中的作用
Gastroenterology. 1996 Sep;111(3):655-65. doi: 10.1053/gast.1996.v111.pm8780570.

幽门螺杆菌胃炎中胃窦和胃体黏膜浸润的CD4(+)淋巴细胞表现出Th1表型。

Antrum- and corpus mucosa-infiltrating CD4(+) lymphocytes in Helicobacter pylori gastritis display a Th1 phenotype.

作者信息

Sommer F, Faller G, Konturek P, Kirchner T, Hahn E G, Zeus J, Röllinghoff M, Lohoff M

机构信息

Institut für Klinische Mikrobiologie, Immunologie und Hygiene der Universität Erlangen-Nürnberg, Erlangen, Germany.

出版信息

Infect Immun. 1998 Nov;66(11):5543-6. doi: 10.1128/IAI.66.11.5543-5546.1998.

DOI:10.1128/IAI.66.11.5543-5546.1998
PMID:9784570
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC108696/
Abstract

In this study, cytokine patterns produced by CD4(+) T cells isolated from antrum or corpus gastral biopsy specimens of 10 patients with Helicobacter pylori-positive gastritis were compared. To this end, expression of intracellular cytokines (interleukin-4 [IL-4] and gamma interferon) and of CD4 was assessed by flow cytometry. Ten to 60% of the isolated CD4(+) T cells produced gamma interferon upon stimulation. With the exception of one patient, IL-4-positive CD4(+) cells were not detected. Therefore, CD4(+) cells infiltrating antrum and corpus stomach mucosa during H. pylori infection show a Th1 phenotype. This polarized Th1-type response may contribute to the inability of the immune system to eradicate H. pylori infection.

摘要

在本研究中,比较了从10例幽门螺杆菌阳性胃炎患者的胃窦或胃体活检标本中分离出的CD4(+) T细胞产生的细胞因子模式。为此,通过流式细胞术评估细胞内细胞因子(白细胞介素-4 [IL-4]和γ干扰素)及CD4的表达。10%至60%的分离出的CD4(+) T细胞在受到刺激后产生γ干扰素。除1例患者外,未检测到IL-4阳性的CD4(+)细胞。因此,幽门螺杆菌感染期间浸润胃窦和胃体黏膜的CD4(+)细胞表现出Th1表型。这种极化的Th1型反应可能导致免疫系统无法根除幽门螺杆菌感染。