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Pathogenicity of Toxoplasma gondii through B‐2 Cell‐Mediated Downregulation of Host Defense Responses
Author(s) -
Mun HyeSeong,
Aosai Fumie,
Chen Mei,
Piao LianXun,
Norose Kazumi,
Iwakura Yoichiro,
Yano Akihiko
Publication year - 2003
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.2003.tb03415.x
Subject(s) - biology , toxoplasma gondii , cd8 , effector , microbiology and biotechnology , cytotoxic t cell , immunology , immune system , in vitro , antibody , biochemistry
IFN‐γ is the primary mediator of anti‐parasite effector mechanisms against Toxoplasma gondii . After intraperitoneal infection with the Fukaya strain of T. gondii , unirradiated IFN‐γ knock‐out (GKO) mice transferred with wild type (WT) CD8 + effector T cells from infected mice failed to induce the production of IFN‐γ and died, whereas irradiated (IR) GKO mice transferred with WT CD8 + T cells induced IFN‐γ production and survived more than 6 months. IR GKO mice transferred with WT CD8 + T cells together with GKO B‐2 cells died 8 days after infection, whereas those transferred with WT CD8 + T cells together with B‐1a or T cells survived. B‐2 cells of infected GKO mice activated CD11b + cells for IL‐4 production, and down‐regulated NO release, STAT1 phosphorylation, and interferon regulatory factor‐1 expression in the peritoneal exudates cells of IR GKO mice transferred with WT CD8 + T cells together with GKO B‐2 cells after infection. Thus, B‐2 cells in T. gondii ‐inf ected mice act as suppressor cells in the host defense of infected mice.