| First Author | Pabbisetty SK | Year | 2014 |
| Journal | Proc Natl Acad Sci U S A | Volume | 111 |
| Issue | 26 | Pages | 9579-84 |
| PubMed ID | 24979767 | Mgi Jnum | J:212159 |
| Mgi Id | MGI:5578245 | Doi | 10.1073/pnas.1323493111 |
| Citation | Pabbisetty SK, et al. (2014) KLF2 is a rate-limiting transcription factor that can be targeted to enhance regulatory T-cell production. Proc Natl Acad Sci U S A 111(26):9579-84 |
| abstractText | Regulatory T cells (Tregs) are a specialized subset of CD4(+) T cells that maintain self-tolerance by functionally suppressing autoreactive lymphocytes. The Treg compartment is composed of thymus-derived Tregs (tTregs) and peripheral Tregs (pTregs) that are generated in secondary lymphoid organs after exposure to antigen and specific cytokines, such as TGF-beta. With regard to this latter lineage, pTregs [and their ex vivo generated counterparts, induced Tregs (iTregs)] offer particular therapeutic potential because these cells can be raised against specific antigens to limit autoimmunity. We now report that transcription factor Kruppel-like factor 2 (KLF2) is necessary for the generation of iTregs but not tTregs. Moreover, drugs that limit KLF2 proteolysis during T-cell activation enhance iTreg development. To the authors' knowledge, this study identifies the first transcription factor to distinguish between i/pTreg and tTreg ontogeny and demonstrates that KLF2 is a therapeutic target for the production of regulatory T cells. |
