Decreased resistance of B cell-deficient mice to infection with Toxoplasma gondii despite unimpaired expression of IFN-γ, TNF-α, and inducible nitric oxide synthase
Decreased resistance of B cell-deficient mice to infection with Toxoplasma gondii despite unimpaired expression of IFN-γ, TNF-α, and inducible nitric oxide synthase
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DOI：
10.4049/jimmunol.164.5.2629
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发表时间：
2000-03-01
影响因子：
4.4
通讯作者：
Suzuki, Y
中科院分区：
文献类型：
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作者：
Kang, H;Remington, JS;Suzuki, Y
用B细胞缺陷（mu MT）小鼠研究了B细胞在抗弓形虫中的作用。经口感染ME 49菌株的10个包囊后，所有mu MT小鼠均在感染的急性期存活，但在感染后3 - 4周死亡。与此相反，所有对照小鼠在感染后8周存活;在此期间，μ MT动物死于感染，寄生虫复制和病理学在它们的大脑中最明显;在它们的肺中也可检测到少量速殖子。与对照小鼠相比，在mu MT小鼠脑中观察到显著更多数量的弓形虫包囊和与速殖子相关的炎症区域，仅在mu MT小鼠脑中观察到与许多速殖子相关的大面积坏死，仅在对照小鼠血清中检测到抗弓形虫IgG抗体，而在两种小鼠血清中检测到相似水平的IFN-γ。IFN-γ，IL 010和诱导型NO合酶在脑中的mRNA量在感染的μ MT和对照小鼠之间没有差异。肿瘤坏死因子-α的mRNA表达在mu MT小鼠的脑中增加。多克隆兔抗T.弓形虫IgG抗体预防了感染的μ MT小鼠脑中与速殖子相关的早期死亡和病理学。这些结果表明，B细胞发挥重要作用，最有可能通过其生产的特定抗体，在抵抗持续活动（速殖子）感染与T。小鼠体内的弓形虫，特别是在大脑和肺部。
The role of B cells in resistance against Toxoplasma gondii was studied using B cell-deficient (mu MT) mice. Following peroral infection with 10 cysts of the ME49 strain, all mu MT mice survived the acute stage of the infection but died between 3 and 4 wk after infection. In contrast, all control mice were alive at 8 wk after infection; At the stage during which mu MT animals succumbed to the infection, parasite replication and pathology were most evident in their brains; small numbers of tachyzoites were also detectable in their lungs. Significantly greater numbers of T, gondii cysts and areas of inflammation associated with tachyzoites were observed in brains of mu MT than in control mice, Large areas of necrosis associated with numerous tachyzoites were observed only in brains of mu MT mice, Anti-T, gondii IgG Abs were detected only in sera of control mice, whereas similar levels of IFN-gamma were detected in sera of both strains of mice. Amounts of mRNA for IFN-gamma, IL010, and inducible NO synthase in the brain did not differ between infected mu MT and control mice. Expression of mRNA for TNF-alpha was increased in brains of mu MT mice. Administration of polyclonal rabbit anti-T. gondii IgG Ab prevented early mortality and pathology associated with tachyzoites in the brain in the infected mu MT mice. These results indicate that B cells play an important role, most likely through their production of specific Abs, in resistance to persistent active (tachyzoite) infection with T. gondii in mice, especially in the brain and lung.