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

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

Copyright © 2011 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 141(2011), 1 vom: 02. Okt., Seite 36-48
1. Verfasser: Mu, Lili (VerfasserIn)
Weitere Verfasser: 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
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2011
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Autoantibodies Cyclooxygenase 2 Inhibitors Cytokines Ligands Myelin Basic Protein Nerve Growth Factors Nitrobenzenes Peptide Fragments mehr... Receptor for Advanced Glycation End Products Receptors, Cholinergic Receptors, Immunologic S100 Calcium Binding Protein beta Subunit S100 Proteins S100b protein, rat Sulfonamides myelin basic protein 68-86 N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 123653-11-2 Cyclooxygenase 2 EC 1.14.99.1 Ptgs2 protein, rat
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245 1 0 |a Activation of the receptor for advanced glycation end products (RAGE) exacerbates experimental autoimmune myasthenia gravis symptoms 
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500 |a published: Print-Electronic 
500 |a CommentIn: Clin Immunol. 2011 Oct;141(1):1-2. - PMID 21889912 
500 |a Citation Status MEDLINE 
520 |a Copyright © 2011 Elsevier Inc. All rights reserved. 
520 |a 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 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 7 |a Autoantibodies  |2 NLM 
650 7 |a Cyclooxygenase 2 Inhibitors  |2 NLM 
650 7 |a Cytokines  |2 NLM 
650 7 |a Ligands  |2 NLM 
650 7 |a Myelin Basic Protein  |2 NLM 
650 7 |a Nerve Growth Factors  |2 NLM 
650 7 |a Nitrobenzenes  |2 NLM 
650 7 |a Peptide Fragments  |2 NLM 
650 7 |a Receptor for Advanced Glycation End Products  |2 NLM 
650 7 |a Receptors, Cholinergic  |2 NLM 
650 7 |a Receptors, Immunologic  |2 NLM 
650 7 |a S100 Calcium Binding Protein beta Subunit  |2 NLM 
650 7 |a S100 Proteins  |2 NLM 
650 7 |a S100b protein, rat  |2 NLM 
650 7 |a Sulfonamides  |2 NLM 
650 7 |a myelin basic protein 68-86  |2 NLM 
650 7 |a N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide  |2 NLM 
650 7 |a 123653-11-2  |2 NLM 
650 7 |a Cyclooxygenase 2  |2 NLM 
650 7 |a EC 1.14.99.1  |2 NLM 
650 7 |a Ptgs2 protein, rat  |2 NLM 
650 7 |a EC 1.14.99.1  |2 NLM 
700 1 |a Zhang, Yao  |e verfasserin  |4 aut 
700 1 |a Sun, Bo  |e verfasserin  |4 aut 
700 1 |a Wang, Jinghua  |e verfasserin  |4 aut 
700 1 |a Xie, Xiaoli  |e verfasserin  |4 aut 
700 1 |a Li, Na  |e verfasserin  |4 aut 
700 1 |a Zhang, Jia  |e verfasserin  |4 aut 
700 1 |a Kong, Qingfei  |e verfasserin  |4 aut 
700 1 |a Liu, Yumei  |e verfasserin  |4 aut 
700 1 |a Han, Zhijuan  |e verfasserin  |4 aut 
700 1 |a Wang, Guangyou  |e verfasserin  |4 aut 
700 1 |a Fu, Zheng  |e verfasserin  |4 aut 
700 1 |a Yu, Bo  |e verfasserin  |4 aut 
700 1 |a Li, Guozhong  |e verfasserin  |4 aut 
700 1 |a Li, Hulun  |e verfasserin  |4 aut 
773 0 8 |i Enthalten in  |t Clinical immunology (Orlando, Fla.)  |d 1999  |g 141(2011), 1 vom: 02. Okt., Seite 36-48  |w (DE-627)NLM098196855  |x 1521-7035  |7 nnns 
773 1 8 |g volume:141  |g year:2011  |g number:1  |g day:02  |g month:10  |g pages:36-48 
856 4 0 |u http://dx.doi.org/10.1016/j.clim.2011.04.013  |3 Volltext 
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