Rutgers Graduate School of Biomedical Sciences, Newark, NJ 07103, USA; Department of Biochemistry and Molecular Biology, Rutgers Biomedical and Health Sciences, New Jersey Medical School - Cancer Center, Newark, NJ 07103, USA.
Rutgers Graduate School of Biomedical Sciences, Newark, NJ 07103, USA; Department of Biochemistry and Molecular Biology, Rutgers Biomedical and Health Sciences, New Jersey Medical School - Cancer Center, Newark, NJ 07103, USA.
Clin Immunol. 2014 May-Jun;152(1-2):140-51. doi: 10.1016/j.clim.2014.03.009. Epub 2014 Mar 24.
B cells represent a critical arm of the adaptive immune system, and under normal circumstances, provide long lasting immunity to a wide range of pathogens. To achieve this, B cells differentiate into specialized subpopulations, which perform unique functions in response to antigen. A complex network of transcription factors regulates this transition as well as subsequent effector functions. Dysregulation of these transcription factors can lead to altered B cell biology and potentially autoimmunity. Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by increased autoantibody production and B cell hyper-reactivity. It still remains unclear, however, what factors contribute to disease pathogenesis. Recent work has suggested dysregulation of B cell transcription factors may play a role in disease onset. Given the prominent role B cells play in the pathogenesis of SLE, it is important to have a full understanding of what transcription factors regulate B cell development, and how dysregulation of some of these transcription factors may contribute to the occurrence and/or pathogenesis of SLE. A comprehensive review of where this field currently stands, what new potential targets have recently been identified, and what functional information is still missing will be discussed.
B 细胞代表了适应性免疫系统的一个关键分支，在正常情况下，它为广泛的病原体提供持久的免疫力。为了实现这一目标，B 细胞分化为专门的亚群，这些亚群在抗原刺激下发挥独特的功能。转录因子的复杂网络调节着这种转变以及随后的效应功能。这些转录因子的失调可导致 B 细胞生物学的改变，并可能导致自身免疫。系统性红斑狼疮（SLE）是一种复杂的自身免疫性疾病，其特征是自身抗体产生增加和 B 细胞过度反应。然而，目前尚不清楚是什么因素导致了疾病的发病机制。最近的研究表明，B 细胞转录因子的失调可能在疾病的发生中起作用。鉴于 B 细胞在 SLE 发病机制中的突出作用，全面了解哪些转录因子调节 B 细胞的发育，以及这些转录因子的失调如何导致 SLE 的发生和/或发病机制，是非常重要的。本文将全面回顾该领域的现状，最近发现了哪些新的潜在靶点，以及仍存在哪些功能信息缺失。
