Altered T-dependent antigen responses and development of autoimmune symptoms in mice lacking E2A in T lymphocytes

作者：Pan LH; Bradney C; Zheng B; Zhuang Y^*

来源：Immunology, 2004, 111(2): 147-154.

DOI：10.1111/j.1365-2567.2003.01802.x

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.

• 出版日期2004-2