| First Author | Mun HS | Year | 2003 |
| Journal | Microbiol Immunol | Volume | 47 |
| Issue | 7 | Pages | 533-42 |
| PubMed ID | 12953847 | Mgi Jnum | J:119064 |
| Mgi Id | MGI:3701065 | Doi | 10.1111/j.1348-0421.2003.tb03415.x |
| Citation | Mun HS, et al. (2003) Pathogenicity of Toxoplasma gondii through B-2 cell-mediated downregulation of host defense responses. Microbiol Immunol 47(7):533-42 |
| abstractText | IFN-gamma is the primary mediator of anti-parasite effector mechanisms against Toxoplasma gondii. After intraperitoneal infection with the Fukaya strain of T. gondii, unirradiated IFN-gamma knock-out (GKO) mice transferred with wild type (WT) CD8+ effector T cells from infected mice failed to induce the production of IFN-gamma and died, whereas irradiated (IR) GKO mice transferred with WT CD8+ T cells induced IFN-y 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-la 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-infected mice act as suppressor cells in the host defense of infected mice. |
