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Molecular orchestration of differentiation and function of regulatory T cells.调节性T细胞分化与功能的分子调控
Genes Dev. 2009 Jun 1;23(11):1270-82. doi: 10.1101/gad.1791009.
2
Innate immune recognition of infected apoptotic cells directs T(H)17 cell differentiation.对感染凋亡细胞的天然免疫识别可引导辅助性T细胞17(TH17)分化。
Nature. 2009 Mar 5;458(7234):78-82. doi: 10.1038/nature07781.
3
Interleukin-17 in host defence against bacterial, mycobacterial and fungal pathogens.白细胞介素-17在宿主抵御细菌、分枝杆菌和真菌病原体中的作用。
Immunology. 2009 Feb;126(2):177-85. doi: 10.1111/j.1365-2567.2008.03017.x.
4
MyD88 signalling plays a critical role in host defence by controlling pathogen burden and promoting epithelial cell homeostasis during Citrobacter rodentium-induced colitis.髓样分化因子88(MyD88)信号传导在宿主防御中发挥关键作用,它通过控制病原菌负荷以及在鼠柠檬酸杆菌诱导的结肠炎期间促进上皮细胞稳态来实现这一作用。
Cell Microbiol. 2008 Mar;10(3):618-31. doi: 10.1111/j.1462-5822.2007.01071.x. Epub 2007 Nov 2.
5
Development of fatal colitis in FVB mice infected with Citrobacter rodentium.感染啮齿柠檬酸杆菌的FVB小鼠发生致命性结肠炎。
Infect Immun. 2007 Jul;75(7):3271-81. doi: 10.1128/IAI.01810-06. Epub 2007 Apr 30.
6
Dual alterations in casein kinase I-epsilon and GSK-3beta modulate beta-catenin stability in hyperproliferating colonic epithelia.酪蛋白激酶I-ε和糖原合成酶激酶-3β的双重改变调节过度增殖的结肠上皮细胞中β-连环蛋白的稳定性。
Am J Physiol Gastrointest Liver Physiol. 2007 Feb;292(2):G599-607. doi: 10.1152/ajpgi.00343.2006. Epub 2006 Oct 19.
7
CD4+CD25+ cell depletion from the normal CD4+ T cell pool prevents tolerance toward the intestinal flora and leads to chronic colitis in immunodeficient mice.从正常CD4+ T细胞库中去除CD4+CD25+细胞会阻止对肠道菌群的耐受,并导致免疫缺陷小鼠发生慢性结肠炎。
Inflamm Bowel Dis. 2006 Jun;12(6):437-46. doi: 10.1097/00054725-200606000-00002.
8
Citrobacter rodentium-induced NF-kappaB activation in hyperproliferating colonic epithelia: role of p65 (Ser536) phosphorylation.柠檬酸杆菌诱导的过度增殖结肠上皮细胞中NF-κB的激活:p65(Ser536)磷酸化的作用
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9
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Critical role of T cell-dependent serum antibody, but not the gut-associated lymphoid tissue, for surviving acute mucosal infection with Citrobacter rodentium, an attaching and effacing pathogen.T细胞依赖性血清抗体而非肠道相关淋巴组织在抵抗鼠柠檬酸杆菌(一种黏附并损毁肠黏膜的病原体)急性黏膜感染中起关键作用。
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鼠艾滋病模型中枸橼酸杆菌诱导的结肠炎。

Citrobacter-induced colitis in mice with murine acquired immunodeficiency syndrome.

机构信息

Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.

出版信息

Vet Pathol. 2010 Mar;47(2):312-7. doi: 10.1177/0300985809358605. Epub 2010 Jan 29.

DOI:10.1177/0300985809358605
PMID:20118320
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3405978/
Abstract

Over the period of a year, colitis was observed in 44 mice raised in a conventional nonspecific pathogen-free colony, 41 of these having concomitant retrovirus-induced murine acquired immunodeficiency syndrome (MAIDS). The lesions varied from bacterial colonization to hyperplasia of colonic mucosa to severe, often fatal, ulceration. Citrobacter rodentium was isolated from the colon and/or liver of 2 mice with colitis. When C57BL/6 mice with or without MAIDS were given graded doses of the bacterium, only those with MAIDS developed colitis, and C rodentium was reisolated from their livers. Thus, mice with MAIDS can develop severe disease following opportunistic infection with an environmental contaminant of the colony that is nonpathogenic for normal adult mice.

摘要

在一年的时间里,在一个常规的非特定病原体无菌群体中饲养的 44 只老鼠中观察到结肠炎,其中 41 只老鼠同时患有逆转录病毒诱导的获得性免疫缺陷综合征(MAIDS)。病变从细菌定植到结肠黏膜增生到严重的、常致命的溃疡不等。从 2 只有结肠炎的老鼠的结肠和/或肝脏中分离出了柠檬酸杆菌。当给予 C57BL/6 老鼠不同剂量的细菌时,只有那些患有 MAIDS 的老鼠发展为结肠炎,并且从它们的肝脏中重新分离出 C 杆状菌。因此,患有 MAIDS 的老鼠在机会性感染无菌群体中的环境污染物后可能会发展为严重疾病,而这种污染物对正常成年老鼠是无毒的。