Peng Stanford L
Clinical Research and Exploratory Development, 3431 Hillview Ave., M/S A2-259, Palo Alto, CA 94304, USA.
Autoimmun Rev. 2009 Jan;8(3):179-83. doi: 10.1016/j.autrev.2008.07.040. Epub 2008 Aug 20.
Systemic lupus erythematosus (SLE) has long been recognized to be characterized by dysregulated signaling pathways in T and B lymphocytes, beginning with observations of cellular hyperactivity and hyperresponsiveness, and evolving to recent studies focused upon the genetic and molecular bases of such phenomena. This review focuses on recently elucidated signaling abnormalities currently thought to be intrinsic to T and/or B cells in human SLE.
系统性红斑狼疮（SLE）长期以来被认为其特征在于T和B淋巴细胞中信号通路失调，最初是观察到细胞的过度活跃和高反应性，随后发展到近期聚焦于此类现象的遗传和分子基础的研究。本综述重点关注目前认为在人类SLE中T和/或B细胞固有的、最近阐明的信号异常。
