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用抗白细胞介素-2抗体治疗后,日本血吸虫感染的小鼠肝纤维化和嗜酸性粒细胞增多症减轻,且CD4 +细胞分泌白细胞介素-5受到选择性抑制。

Schistosoma japonicum-infected mice show reduced hepatic fibrosis and eosinophilia and selective inhibition of interleukin-5 secretion by CD4+ cells after treatment with anti-interleukin-2 antibodies.

作者信息

Cheever A W, Xu Y, Sher A, Finkelman F D, Cox T M, Macedonia J G

机构信息

Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892.

出版信息

Infect Immun. 1993 Apr;61(4):1288-92. doi: 10.1128/iai.61.4.1288-1292.1993.

Abstract

Schistosoma japonicum-infected mice were injected with antibodies to interleukin-2 (IL-2) and/or IL-2 receptor to clarify the role of IL-2 on the granulomatous reaction around schistosome eggs in the liver. Granulomas were of normal or slightly increased size in animals subjected to IL-2 blockade, but hepatic fibrosis was markedly decreased in treated animals 10 weeks after infection. Anti-IL-2 treatment significantly decreased the in vitro secretion of IL-5 by antigen-stimulated spleen cells, and peripheral eosinophilia and tissue eosinophilia were diminished. Secretion of IL-2, IL-4, and gamma interferon was unaffected. Our results indicate that IL-2 is not an essential determinant of granuloma size in S. japonicum-infected mice but that, as in Schistosoma mansoni infection, the development of hepatic fibrosis is critically dependent on IL-2 levels and granuloma size and hepatic fibrosis are differentially regulated.

摘要

给感染日本血吸虫的小鼠注射白细胞介素-2(IL-2)抗体和/或IL-2受体抗体,以阐明IL-2在肝脏中血吸虫卵周围肉芽肿反应中的作用。在接受IL-2阻断的动物中,肉芽肿大小正常或略有增加,但在感染后10周接受治疗的动物中,肝纤维化明显减轻。抗IL-2治疗显著降低了抗原刺激的脾细胞体外分泌IL-5的水平,外周嗜酸性粒细胞增多症和组织嗜酸性粒细胞增多现象减少。IL-2、IL-4和γ干扰素的分泌未受影响。我们的结果表明,IL-2不是感染日本血吸虫小鼠肉芽肿大小的必要决定因素,但与曼氏血吸虫感染一样,肝纤维化的发展严重依赖于IL-2水平,且肉芽肿大小和肝纤维化受到不同的调节。

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The role of cytokines in the pathogenesis of hepatic granulomatous disease in Schistosoma mansoni infected mice.
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本文引用的文献

6
Dynamics of collagen accumulation and polymorphism in murine Schistosoma japonicum.
Gastroenterology. 1985 Sep;89(3):617-24. doi: 10.1016/0016-5085(85)90459-7.

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