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Altered T‐dependent antigen responses and development of autoimmune symptoms in mice lacking E2A in T lymphocytes
Author(s) -
Pan Lihua,
Bradney Curtis,
Zheng Biao,
Zhuang Yuan
Publication year - 2004
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.0019-2805.2003.01802.x
Subject(s) - t cell receptor , biology , t cell , effector , immunology , microbiology and biotechnology , antigen , cytotoxic t cell , immune system , genetics , in vitro
Summary 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 naïve and effector T cells. In the absence of E2A, TCR‐induced proliferation is increased in naïve 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.