| First Author | Oestreich KJ | Year | 2014 |
| Journal | Nat Immunol | Volume | 15 |
| Issue | 10 | Pages | 957-64 |
| PubMed ID | 25194422 | Mgi Jnum | J:259361 |
| Mgi Id | MGI:6142282 | Doi | 10.1038/ni.2985 |
| Citation | Oestreich KJ, et al. (2014) Bcl-6 directly represses the gene program of the glycolysis pathway. Nat Immunol 15(10):957-64 |
| abstractText | Despite the increasing knowledge of the molecular events that induce the glycolysis pathway in effector T cells, very little is known about the transcriptional mechanisms that dampen the glycolysis program in quiescent cell populations such as memory T cells. Here we found that the transcription factor Bcl-6 directly repressed genes encoding molecules involved in the glycolysis pathway, including Slc2a1, Slc2a3, Pkm and Hk2, in type 1 helper T cells (TH1 cells) exposed to low concentrations of interleukin 2 (IL-2). Thus, Bcl-6 had a role opposing the IL-2-sensitive glycolytic transcriptional program that the transcription factors c-Myc and HIF-1alpha promote in effector T cells. Additionally, the TH1 lineage-specifying factor T-bet functionally antagonized the Bcl-6-dependent repression of genes encoding molecules in the glycolysis pathway, which links the molecular balance of these two factors to regulation of the metabolic gene program. |
