12a(综述,在人类SLE中IL-2转录受抑).pdfVIP

Autoimmunity Reviews 5 (2006) 118–121 /locate/autrev Transcriptional repression of interleukin-2 in human systemic lupus erythematosus Christina G. Katsiari a,*, George C. Tsokos a,b a Dept. of Cellular Injury, Walter Reed Army Institute of Research, Silver Spring, MD 20190, USA b Department of Medicine, Uniformed Services University, Bethesda, MD 20814, USA Available online 26 September 2005 Abstract T cells from patients with SLE produce decreased amounts of interleukin-2 (IL-2), a central cytokine in the regulation of the immune response. We discuss herein the abnormalities underlying IL-2 deficiency in SLE T cells. D 2005 Elsevier B.V. All rights reserved. Keywords: Systemic lupus erythematosus; Interleukin-2; Transcriptional regulation 1. Introduction [3]. The function of these transcription factors depends on the activation state of the cell. Engagement of the Interleukin-2 (IL-2) is essential for both the promo- TCR/CD3 complex, especially in the presence of a co- tion and the suppression of the immune response [1]. T stimulatory signal (e.g. via CD28), triggers a cascade of cells from patients and mice with SLE produce de- biochemical events (e.g. rise of intracellular calcium), creased amounts of IL-2, which is believed to contrib- which result in the activation of kinases, such as PKC ute to increased susceptibility to infections,