| First Author | Sullivan BM | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 7 | Pages | 4593-602 |
| PubMed ID | 16177104 | Mgi Jnum | J:118949 |
| Mgi Id | MGI:3700860 | Doi | 10.4049/jimmunol.175.7.4593 |
| Citation | Sullivan BM, et al. (2005) Increased susceptibility of mice lacking T-bet to infection with Mycobacterium tuberculosis correlates with increased IL-10 and decreased IFN-gamma production. J Immunol 175(7):4593-602 |
| abstractText | A sustained CD4+ Th1-dominated type 1 immune response is required to successfully control Mycobacterium tuberculosis infection. Considerable work has demonstrated that the transcription factor, T-bet, is required for IFN-gamma expression and fundamental to the generation of type 1 immunity in multiple cell types. Mice lacking T-bet are susceptible to virulent M. tuberculosis infection. Susceptibility of T-bet-deficient mice is associated with increased systemic bacterial burden, diminished IFN-gamma production, and the striking accumulation of eosinophilic macrophages and multinucleated giant cells in the lung. Interestingly, T-bet(-/-) mice did not develop a fully polarized Th2 response toward M. tuberculosis, but exhibited selective elevation of IL-10 production. These results indicate that T-bet plays a central role in controlling M. tuberculosis disease progression, in part through the regulation of both IFN-gamma and IL-10. |
