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Mice lack of LRG-47 display the attenuated outcome of infection with Schistosoma japonicum
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  • 作者:Yanan Gao ; Jingjiao Wu ; Meijuan Zhang ; Min Hou ; Minjun Ji
  • 关键词:Schistosoma japonicum ; p47 GTPases ; LRG ; 47 ; Immune response
  • 刊名:Parasitology Research
  • 出版年:2016
  • 出版时间:March 2016
  • 年:2016
  • 卷:115
  • 期:3
  • 页码:1185-1193
  • 全文大小:1,598 KB
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  • 作者单位:Yanan Gao (1) (3)
    Jingjiao Wu (1) (4)
    Meijuan Zhang (1)
    Min Hou (1)
    Minjun Ji (1) (2)

    1. Department of Pathogen Biology, Nanjing Medical University, Nanjing, Jiangsu, 210029, China
    3. College of Basic Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China
    4. Department of Basic Medical Sciences, School of Medicine, Tsinghua University, Beijing, China
    2. Jiangsu Province Key Laboratory of Modern Pathogen Biology, Nanjing, Jiangsu, China
  • 刊物类别:Biomedical and Life Sciences
  • 刊物主题:Biomedicine
    Medical Microbiology
    Microbiology
    Immunology
  • 出版者:Springer Berlin / Heidelberg
  • ISSN:1432-1955
文摘
Interferon-inducible GTPase LRG-47 (also named immune-related GTPase M, Irgm1) is a member of the p47 GTPase family that has been shown to regulate host resistance to intracellular pathogens. Little knowledge has been known about the role of LRG-47 in host’s responses to extracellular pathogens. To investigate possible roles of LRG-47 in the course of Schistosoma japonicum infection, LRG-47-deficient (LRG-47−/−) and wild-type (WT) mice were challenged with cercariae of S. japonicum, and the cellular and humoral responses in mice were analyzed. At the acute stage of S. japonicum infection, in contrast to WT mice, LRG-47−/− mice showed the significantly decreased egg burden, low schistosome-specific antibody response, and the decreased Th1 and increased Tc1 responses. Additionally, Schistosoma japonicum-specific egg antigen immunization also produced the similar humoral and cellular immune responses as S. japonicum infection. Taken together, these data suggested that the deficiency of LRG-47 might affect host’s CD4+ T cell immune response via the weakening of IFN-γ downstream signaling; however, the specific function of LRG-47 on dealing with extracellular worm needs to be further studied.

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