EGR-2 Is Not Required for In Vivo CD4 T Cell Mediated Immune Responses
EGR-2 Is Not Required for In Vivo CD4 T Cell Mediated Immune Responses
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DOI：
10.1371/journal.pone.0012904
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发表时间：
2010-09-23
期刊：
影响因子：
3.7
通讯作者：
Turka, Laurence A.
中科院分区：
文献类型：
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作者：
Ramon, Hilda E.;Cejas, Pedro J.;Turka, Laurence A.
背景：锌指转录因子EGR-2在诱导T细胞能量和调节外周T细胞耐受性中发挥重要作用。在体外，先前的一项研究表明，缺乏EGR-2的T细胞对IL-2具有超增殖作用，并产生高水平的效应细胞因子ifn - γ。EGR-2缺陷小鼠外周血淋巴器官中CD44（高）T细胞水平升高，随着年龄增长，出现自身免疫样特征。主要发现：本研究表明，尽管携带活化CD44（高）CD62L（低）表型的细胞数量增加，但来自年轻健康EGR-2缺陷小鼠的T细胞具有正常的增殖和细胞因子反应，并且小鼠自身对次要组织相容性抗原、病原体弓形虫和淋巴细胞性脉络膜脑膜炎病毒产生正常的免疫反应。结论：我们的研究结果表明，EGR-2并不需要对外来抗原产生正常的急性体内免疫反应，相反，它可能有助于调节对慢性抗原暴露的反应，例如发生在自身抗原上的反应。
Background: The zinc finger transcription factor EGR-2 has been shown to play an important role in the induction of T cell anergy and the regulation of peripheral T cell tolerance. In vitro, a prior study has show that T cells deficient in EGR-2 are hyperproliferative to IL-2 and produce elevated levels of the effector cytokine IFN-gamma. EGR-2 deficient mice have increased levels of CD44(high) T cells in peripheral lymphoid organs, and with age, develop autoimmune-like features.Principal Findings: Here we show that despite increased numbers of cells bearing an activated CD44(high) CD62L(low) phenotype, T cells from young healthy EGR-2 deficient mice have normal proliferative and cytokine responses, and the mice themselves mount normal immune responses against minor histocompatibility antigens, and the pathogens Toxoplasma gondii and lymphocytic choriomeningitis virus.Conclusions: Our results indicate that EGR-2 is not required to mount normal acute in vivo immune responses against foreign antigens, and suggest instead that it may serve to regulate the response to chronic antigenic exposure, such as that which occurs to autoantigens.