期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2014
卷号：111
期号：46
页码：16484-16489
DOI：10.1073/pnas.1417215111
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：SignificanceEarly growth response 2 (EGR2) is a transcription factor that can negatively regulate T-cell activation. We unexpectedly found that EGR2 promotes peripheral naive T-cell proliferation and differentiation, with less T-cell receptor-induced IL-2 production in Egr2-deficient naive T cells and diminished cytokine production in T-helper differentiated cells. Moreover, EGR2 was required for T-cell responses to influenza, with delayed viral clearance and more severe pathology in lungs of Egr2 conditional knockout mice, as well as decreased effector cytokine production from T cells. Thus, EGR2 can act as a positive regulator essential for a normal T-cell response to viral infection, a finding with potential clinical implications. Early growth response 2 (EGR2) transcription factor negatively regulates T-cell activation, in contrast to the positive regulation of this process by EGR1. Here, we unexpectedly found that EGR2 promotes peripheral naive T-cell differentiation, with delayed T-cell receptor-induced proliferation in naive T cells from Egr2 conditional knockout (CKO) mice and decreased production of IFN-{gamma
关键词：EGR2 ; T cells ; differentiation ; RNA-Seq ; influenza
