| First Author | Dai WJ | Year | 2004 |
| Journal | Immunology | Volume | 112 |
| Issue | 3 | Pages | 481-8 |
| PubMed ID | 15196217 | Mgi Jnum | J:90911 |
| Mgi Id | MGI:3045500 | Doi | 10.1111/j.1365-2567.2004.01885.x |
| Citation | Dai WJ, et al. (2004) Echinococcus multilocularis proliferation in mice and respective parasite 14-3-3 gene expression is mainly controlled by an alphabeta CD4 T-cell-mediated immune response. Immunology 112(3):481-8 |
| abstractText | The role of specific B lymphocytes and T-cell populations in the control of experimental Echinococus multilocularis infection was studied in micro MT, nude, T-cell receptor (TCR)-beta(-/-), major histocompatibility complex (MHC)-I(-/-) and MHC-II(-/-) mice. At 2 months postinfection, the parasite mass was more than 10 times higher in nude, TCR-beta(-/-) and MHC-II(-/-) mice than in infected C57BL/6 wild-type (WT) mice, and these T-cell-deficient mice started to die of the high parasite load at this time-point. In contrast, MHC-I(-/-) and micro MT mice exhibited parasite growth rates similar to those found in WT controls. These findings clearly point to the major role that CD4(+) alphabeta(+) T cells play in limiting the E. multilocularis proliferation, while CD8(+) T and B cells appeared to play a minor role in the control of parasite growth. In the absence of T cells, especially CD4(+) or alphabeta(+) T cells, the cellular immune response to infection was impaired, as documented by the lack of hepatic granuloma formation around the parasite and by a decreased splenocyte responsiveness to concanavalin A (Con A) and parasite antigen stimulation. Surprisingly, in T-cell-deficient mice, the ex vivo expression of interferon-gamma (IFN-gamma) and other inflammatory cytokines (except for interleukin-6) were increased in association with a high parasite load. Thus, the relative protection mediated by CD4(+) alphabeta(+) T cells against E. multilocularis infection seemed not be IFN-gamma dependent, but rather to rely on the effector's function of CD4(+) alphabeta(+) T cells. The local restriction of parasite germinal cell proliferation was reflected by a regulatory effect on the expression of 14-3-3 protein within the parasite tissue in T-cell-deficient mice. These results provide a strong indication that the CD4(+) alphabeta(+) T-cell-mediated immune response contributes to the control of the parasite growth and to the regulation of production of the parasite 14-3-3 protein in metacestode tissues. |
