鸟分枝杆菌肉芽肿免疫介导坏死的遗传控制
Genetic control of immune-mediated necrosis of Mycobacterium avium granulomas.
作者信息
Flórido Manuela, Appelberg Rui
机构信息
Laboratory of Microbiology and Immunology of Infection, Institute for Molecular and Cell Biology, University of Porto, Portugal.
出版信息
Immunology. 2006 May;118(1):122-30. doi: 10.1111/j.1365-2567.2006.02350.x.
Abstract
Intravenous infection of C57BL/6 and C57BL/10 mice with low doses of a highly virulent strain of Mycobacterium avium (ATCC 25291) led to the development of granulomas that underwent necrosis. In contrast, neither BALB/c nor DBA/1 mice developed granuloma necrosis after such infection despite a similar course of mycobacterial proliferation. Studies with C57BL/10 mice congenic for the Hc locus revealed that an intact complement C5 gene is required for granuloma necrosis. On the other hand, genetic disruption of the interleukin-10 gene in BALB/c mice made this strain susceptible to granuloma necrosis.
摘要
用低剂量高毒力鸟分枝杆菌菌株（ATCC 25291）对C57BL/6和C57BL/10小鼠进行静脉感染，会导致肉芽肿形成并发生坏死。相比之下，BALB/c和DBA/1小鼠在这种感染后虽有相似的分枝杆菌增殖过程，但均未发生肉芽肿坏死。对Hc位点同基因的C57BL/10小鼠的研究表明，肉芽肿坏死需要完整的补体C5基因。另一方面，BALB/c小鼠白细胞介素-10基因的基因破坏使该品系易发生肉芽肿坏死。
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