| First Author | D'Cruz LM | Year | 2012 |
| Journal | Eur J Immunol | Volume | 42 |
| Issue | 8 | Pages | 2031-41 |
| PubMed ID | 22585759 | Mgi Jnum | J:187854 |
| Mgi Id | MGI:5438455 | Doi | 10.1002/eji.201242497 |
| Citation | D'Cruz LM, et al. (2012) Loss of E protein transcription factors E2A and HEB delays memory-precursor formation during the CD8+ T-cell immune response. Eur J Immunol 42(8):2031-41 |
| abstractText | The transcription factors E2A and HEB (members of the E protein family) have been shown to play essential roles in lymphocyte development, while their negative regulators, the Id proteins, have been implicated in both lymphocyte development and in the CD8(+) T-cell immune response. Here, we show that E proteins also influence CD8(+) T cells responding to infection. E protein expression was upregulated by CD8(+) T cells during the early stages of infection and increased E protein DNA-binding activity could be detected upon TCR stimulation. Deficiency in the E proteins, E2A and HEB, led to increased frequency of terminally differentiated effector KLRG1(hi) CD8(+) T cells in mice during infection, and decreased generation of longer-lived memory-precursor cells during the immune response. These data suggest a model whereby E protein transcription factor activity favors rapid memory-precursor T-cell formation while their negative regulators, Id2 and Id3, are both required for robust effector CD8(+) T-cell response during infection. |
