Other
13 Authors
- Guo L,
- Yagi R,
- Wei G,
- Feigenbaum L,
- Punkosdy G,
- Oler AJ,
- Paul WE,
- Zhu J,
- Zhao K,
- Yamane H,
- Jankovic D,
- Sharma S,
- Hu G
| First Author | Zhu J | Year | 2012 |
| Journal | Immunity | Volume | 37 |
| Issue | 4 | Pages | 660-73 |
| PubMed ID | 23041064 | Mgi Jnum | J:188559 |
| Mgi Id | MGI:5441110 | Doi | 10.1016/j.immuni.2012.09.007 |
| Citation | Zhu J, et al. (2012) The Transcription Factor T-bet Is Induced by Multiple Pathways and Prevents an Endogenous Th2 Cell Program during Th1 Cell Responses. Immunity 37(4):660-73 |
| abstractText | T-bet is a critical transcription factor for T helper 1 (Th1) cell differentiation. To study the regulation and functions of T-bet, we developed a T-bet-ZsGreen reporter mouse strain. We determined that interleukin-12 (IL-12) and interferon-gamma (IFN-gamma) were redundant in inducing T-bet in mice infected with Toxoplasma gondii and that T-bet did not contribute to its own expression when induced by IL-12 and IFN-gamma. By contrast, T-bet and the transcription factor Stat4 were critical for IFN-gamma production whereas IFN-gamma signaling was dispensable for inducing IFN-gamma. Loss of T-bet resulted in activation of an endogenous program driving Th2 cell differentiation in cells expressing T-bet-ZsGreen. Genome-wide analyses indicated that T-bet directly induced many Th1 cell-related genes but indirectly suppressed Th2 cell-related genes. Our study revealed redundancy and synergy among several Th1 cell-inducing pathways in regulating the expression of T-bet and IFN-gamma, and a critical role of T-bet in suppressing an endogenous Th2 cell-associated program. |
