论文库首页  论文库
 
论文编号:
论文题目: The Anti-Spasticity Drug Baclofen Alleviates Collagen-induced Arthritis and Regulates Dendritic Cells
英文论文题目: The Anti-Spasticity Drug Baclofen Alleviates Collagen-induced Arthritis and Regulates Dendritic Cells
第一作者: Huang, SC; Mao, JX; Wei, B; Pei, G
英文第一作者: Huang, SC; Mao, JX; Wei, B; Pei, G
联系作者: Huang, SC (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, 320 Yue Yang Rd, Shanghai 200031, Peoples R China.
英文联系作者: Huang, SC (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, 320 Yue Yang Rd, Shanghai 200031, Peoples R China.
外单位作者单位:
英文外单位作者单位:
发表年度: 2015
卷: 230
期: 7
页码: 1438-1447
摘要: Baclofen is used clinically as a drug that treats spasticity, which is a syndrome characterized by excessive contraction of the muscles and hyperflexia in the central nervous system (CNS), by activating GABA(B) receptors (GABA(B)Rs). Baclofen was recently reported to desensitize chemokine receptors and to suppress inflammation through the activation of GABA(B)Rs. GABA(B)Rs are expressed in various immune cells, but the functions of these receptors in autoimmune diseases remain largely unknown. In this study, we investigated the effects of baclofen in murine collagen-induced arthritis (CIA). Oral administration of baclofen alleviated the clinical development of CIA, with a reduced number of IL-17-producing T helper 17 (T(H)17) cells. In addition, baclofen treatment suppressed dendritic cell (DC)-primed T(H)17 cell differentiation by reducing the production of IL-6 by DCs in vitro. Furthermore, the pharmacological and genetic blockade of GABA(B)Rs in DCs weakened the effects of baclofen, indicating that GABA(B)Rs are the molecular targets of baclofen on DCs. Thus, our findings revealed a potential role for baclofen in the treatment of CIA, as well as a previously unknown signaling pathway that regulates DC function. J. Cell. Physiol. 230: 1438-1447, 2015. (c) 2015 Wiley Periodicals, Inc., A Wiley Company
英文摘要: Baclofen is used clinically as a drug that treats spasticity, which is a syndrome characterized by excessive contraction of the muscles and hyperflexia in the central nervous system (CNS), by activating GABA(B) receptors (GABA(B)Rs). Baclofen was recently reported to desensitize chemokine receptors and to suppress inflammation through the activation of GABA(B)Rs. GABA(B)Rs are expressed in various immune cells, but the functions of these receptors in autoimmune diseases remain largely unknown. In this study, we investigated the effects of baclofen in murine collagen-induced arthritis (CIA). Oral administration of baclofen alleviated the clinical development of CIA, with a reduced number of IL-17-producing T helper 17 (T(H)17) cells. In addition, baclofen treatment suppressed dendritic cell (DC)-primed T(H)17 cell differentiation by reducing the production of IL-6 by DCs in vitro. Furthermore, the pharmacological and genetic blockade of GABA(B)Rs in DCs weakened the effects of baclofen, indicating that GABA(B)Rs are the molecular targets of baclofen on DCs. Thus, our findings revealed a potential role for baclofen in the treatment of CIA, as well as a previously unknown signaling pathway that regulates DC function. J. Cell. Physiol. 230: 1438-1447, 2015. (c) 2015 Wiley Periodicals, Inc., A Wiley Company
刊物名称: JOURNAL OF CELLULAR PHYSIOLOGY
英文刊物名称: JOURNAL OF CELLULAR PHYSIOLOGY
论文全文:
英文论文全文:
全文链接:
其它备注:
英文其它备注:
学科: Cell Biology; Physiology
英文学科: Cell Biology; Physiology
影响因子: 3.839
第一作者所在部门:
英文第一作者所在部门:
论文出处:
英文论文出处:
论文类别: Article
英文论文类别: Article
参与作者:
英文参与作者:
 
2014 中国科学院上海生命科学研究院 版权所有