Induction of granulomas in interferon-gamma gene-disrupted mice by avirulent but not by virulent strains of Mycobacterium tuberculosis.
Induction of granulomas in interferon-gamma gene-disrupted mice by avirulent but not by virulent strains of Mycobacterium tuberculosis.
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无毒力而非强毒力的结核分枝杆菌菌株可在干扰素-γ基因破坏的小鼠中诱导肉芽肿。
DOI：
--
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发表时间：
1998
影响因子：
3
通讯作者：
Y. Iwakura
中科院分区：
文献类型：
--
作者：
I. Sugawara;H. Yamada;Y. Kazumi;N. Doi;K. Otomo;T. Aoki;S. Mizuno;T. Udagawa;Y. Tagawa;Y. Iwakura
为了更好地了解干扰素-γ在特异性肉芽肿形成中的病理作用，我们建立了干扰素-γ基因缺陷小鼠(BALB/c和C57BL/6)。通过同源重组将β-半乳糖苷酶基因(LacZ)和新霉素抗性基因(Neo)插入到胚胎干细胞(ES)的翻译起始点，从而打乱了胚胎干细胞中的干扰素-γ基因。将6周龄的干扰素-γ缺陷型和野生型小鼠经尾静脉接种结核分枝杆菌(Kurono、H37Rv、H37Ra和BCG巴斯德)10(3)-10(7)株。7周后，对小鼠进行肉芽肿形成检查。无毒卡介苗巴斯德和H37Ra菌株(10(3)-10(4)杆菌/毫升)可在干扰素-γ基因缺陷小鼠的脾、肝和肺引起肉芽肿。肉芽肿由上皮样巨噬细胞和朗汉多核巨细胞组成，但无干酪样坏死。强毒株Kurono和H37Rv可引起干扰素-γ基因缺陷小鼠各脏器的播散性脓肿，但不能引起肉芽肿，脓肿病灶中未检测到Mac-3阳性巨噬细胞。这些结果表明，干扰素-γ可能是巨噬细胞活化的主要原因，其他因素(S)可能参与了肉芽肿的形成机制。
To gain a better understanding of the pathological role of interferon-gamma (IFN-gamma) in specific granuloma formation, IFN-gamma gene-deficient mice (BALB/c and C57BL/6) were produced. The IFN-gamma gene in embryonic stem (ES) cells was disrupted by inserting the beta-galactosidase gene (lacZ) and the neomycin resistance gene (neo) at the translation initiation site in exon 1 by homologous recombination. Six-week-old IFN-gamma-deficient and wild-type mice were inoculated with 10(3)-10(7) bacilli of various strains of Mycobacterium tuberculosis (Kurono, H37Rv, H37Ra and BCG Pasteur) through their tail veins. The mice were examined 7 weeks later for granuloma formation. The avirulent BCG Pasteur and H37Ra strains (10(3)-10(4) bacilli/ml) induced granulomas in the spleen, liver and lungs of IFN-gamma-deficient mice. The granulomas consisted of epithelioid macrophages and Langhans multinucleate giant cells, but lacked caseous necrosis. The virulent Kurono and H37Rv strains induced disseminated abscesses but not granulomas in various organs of IFN-gamma-deficient mice and Mac-3-positive macrophages were not detected in the abscess lesions. These results suggest that IFN-gamma may be primarily responsible for macrophage activation and that other factor(s) may be involved in the granuloma formation mechanism.
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应激蛋白是麻风病和结核病的免疫靶标。
DOI：
10.1073/pnas.85.12.4267
发表时间：
1988
影响因子：
11.1
作者：
Young,D;Lathigra,R;Hendrix,R;Sweetser,D;Young,RA
通讯作者：
Young,RA
影响因子：
4.4
作者：
Peter F. Barnes;S. Fong;Patrick J. Brennan;P. Twomey;A. Mazumder;R. Modlin
通讯作者：
Peter F. Barnes;S. Fong;Patrick J. Brennan;P. Twomey;A. Mazumder;R. Modlin
获得性免疫缺陷综合征中淋巴因子和免疫（γ）干扰素的产生受损。
DOI：
10.1056/nejm198404053101404
发表时间：
1984
期刊：
The New England journal of medicine
影响因子：
--
作者：
Murray,HW;Rubin,BY;Masur,H;Roberts,RB
通讯作者：
Roberts,RB
巨噬细胞分化抗原在小鼠细胞系上的体外表达和诱导。
DOI：
--
发表时间：
1983
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Ralph,P;Ho,MK;Litcofsky,PB;Springer,TA
通讯作者：
Springer,TA