ID 29079
Author
Nakano, Yoko Department of Parasitology and Immunology, The University of Tokushima School of Medicine
Hisaeda, Hajime Department of Parasitology and Immunology, The University of Tokushima School of Medicine
Sakai, Tohru Department of Parasitology and Immunology, The University of Tokushima School of Medicine Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Zhang, Manxin Department of Parasitology and Immunology, The University of Tokushima School of Medicine
Maekawa, Yoichi Department of Parasitology and Immunology, The University of Tokushima School of Medicine
Zhang, Tianqian Department of Parasitology and Immunology, The University of Tokushima School of Medicine
Himeno, Kunisuke Department of Parasitology and Immunology, The University of Tokushima School of Medicine
Keywords
Toxoplasma gondii
HSP65
NKT cells
Content Type
Journal Article
Description
The intraperitoneal infection with Toxoplasma gondii (T. gondii) caused accumulation of γδ T, NK, NK1.1+T-like (NKT) cells at inflamed sites. To clarify the roles of these cells in protection against T. gondii at the inflamed sites, BALB/c mice were depleted of γδ T, NK, NK and NKT cells by treatment with antibody against TCR-γδ, asialoGM1 or Interleukin-2 receptor β-chain (IL-2Rβ), respectively, prior to infection. Mice treated with anti-TCR-γδ monoclonal antibody (mAb) became more susceptible to infection, whereas mice treated with anti-IL-2Rβ mAb acquired resistance. Treatment with anti-asialoGM1 Ab showed no effect. We previously reported that heat shock protein 65 (HSP65) in macrophages induced by γδ T cells plays an essential role in protective immunity against T. gondii infection, by preventing apoptotic death of infected macrophages. In the present study, we showed that treatment with anti-IL-2Rβ mAb, but not with anti-asialoGM1 Ab, enhanced the HSP65 induction in macrophages, and inhibited Interleukin-4 (IL-4) expression in nonadherent peritoneal exudate cells. Furthermore, neutralization of endogenous IL-4 by anti-IL-4 mAb enhanced the HSP65 induction in macrophages. These findings suggest that NKT cells, but not NK cells, negatively regulate the protective immunity against T. gondii infection possibly by producing IL-4and suppressing HSP65 induction.
Journal Title
The journal of medical investigation : JMI
ISSN
13431420
NCID
AA11166929
Volume
48
Issue
1-2
Start Page
73
End Page
80
Sort Key
73
Published Date
2001
Remark
EDB ID
FullText File
language
eng
departments
Medical Sciences