| First Author | Pan L | Year | 2004 |
| Journal | Immunology | Volume | 111 |
| Issue | 2 | Pages | 147-54 |
| PubMed ID | 15027899 | Mgi Jnum | J:88415 |
| Mgi Id | MGI:3033249 | Doi | 10.1111/j.0019-2805.2003.01802.x |
| Citation | Pan L, et al. (2004) Altered T-dependent antigen responses and development of autoimmune symptoms in mice lacking E2A in T lymphocytes. Immunology 111(2):147-54 |
| abstractText | E2A has been shown to be an important transcription factor downstream of the T-cell receptor (TCR) signal during T-cell development. The TCR signal is known to elicit different cellular responses at different stages of T-cell development. Whether E2A is still required for normal TCR signalling in mature T cells is unknown. Here we examined T-cell function after disruption of the E2A gene exclusively in the T-cell lineage. The conditional E2A-deficient mice show enhanced humoral immunity to a T-dependent antigen. We further show that E2A is involved in regulating TCR-induced T-cell proliferation events. However, E2A seems to play opposite roles in naive and effector T cells. In the absence of E2A, TCR-induced proliferation is increased in naive T cells and decreased in effector T cells. At older ages, these mice frequently develop antinuclear antibodies and proteinuria. Our studies suggest that E2A regulates T-cell function and the loss of E2A may promote age-dependent autoimmune diseases. |
