Activation of the receptor for advanced glycation end products (RAGE) exacerbates experimental autoimmune myasthenia gravis symptoms

CORC > 厦门大学 > 生命科学－已发表论文

	Activation of the receptor for advanced glycation end products (RAGE) exacerbates experimental autoimmune myasthenia gravis symptoms
	Mu, Lili ; Zhang, Yao ; Sun, Bo ; Wang, Jinghua ; Xie, Xiaoli ; Li, Na ; Zhang, Jia ; Kong, Qingfei ; Liu, Yumei ; Han, Zhijuan ; Wang, Guangyou ; Fu, Zheng ; Yu, Bo ; Li, Guozhong ; Li, Hulun ; Fu Z(付正)
刊名	http://dx.doi.org/10.1016/j.clim.2011.04.013
	2011-10
关键词	REGULATORY T-CELLS INTERFERON-GAMMA ALZHEIMERS-DISEASE IFN-GAMMA B-CELLS MICE BLOCKADE CYCLOOXYGENASE-2 IMMUNOREGULATION IDENTIFICATION
英文摘要	National Nature Science Foundation of China [30770665, 81000511, 30901330]; China Postdoctoral Science Foundation [20100480062]; Harbin Medical University cell biological engineering center [1151gzx05]; Harbin Science Et Technology Bureau [2008RFQXS085];; RAGE belongs to immunoglobulin superfamily and serves as a ligand for various immunoregulatory molecules including S100B that has been demonstrated important to T cell mediated autoimmune diseases. In this context, we hypothesized that RAGE could also impact B cell mediated, T cell-dependent autoimmune diseases. This was tested using myasthenia gravis (MG) animal model, EAMG. We show that expression of both RAGE and S100B are increased during EAMG and the interaction between RAGE and S100B affected the Th1/Th2/Th17/Treg cell equilibrium, up-regulate AChR-specific T cell proliferation. Furthermore, addition of S100B in vitro stimulated splenocyte activity linked to COX-2 up-regulation. NS-398, a selective COX-2 inhibitor, effectively diminished S100B mediated activity of AChR-specific antibody secreting splenocytes. These findings suggested that a reciprocal relationship between RAGE and S100B promoted the development of EAMG, highlighting the importance of understanding the mechanisms of EAMG disease as a means of developing new therapies for the treatment of MG. (C) 2011 Elsevier Inc. All rights reserved.
语种	英语
出版者	CLIN IMMUNOL
内容类型	期刊论文
源URL	[http://dspace.xmu.edu.cn/handle/2288/90502]
专题	生命科学－已发表论文
推荐引用方式 GB/T 7714	Mu, Lili,Zhang, Yao,Sun, Bo,et al. Activation of the receptor for advanced glycation end products (RAGE) exacerbates experimental autoimmune myasthenia gravis symptoms[J]. http://dx.doi.org/10.1016/j.clim.2011.04.013,2011.
APA	Mu, Lili.,Zhang, Yao.,Sun, Bo.,Wang, Jinghua.,Xie, Xiaoli.,...&付正.(2011).Activation of the receptor for advanced glycation end products (RAGE) exacerbates experimental autoimmune myasthenia gravis symptoms.http://dx.doi.org/10.1016/j.clim.2011.04.013.
MLA	Mu, Lili,et al."Activation of the receptor for advanced glycation end products (RAGE) exacerbates experimental autoimmune myasthenia gravis symptoms".http://dx.doi.org/10.1016/j.clim.2011.04.013 (2011).