发明授权
US08916525B2 TNF-A and TWEAK dual antagonist for the prophylaxis and treatment of autoimmune diseases
有权
TNF-A和TWEAK双重拮抗剂用于预防和治疗自身免疫性疾病
- 专利标题： TNF-A and TWEAK dual antagonist for the prophylaxis and treatment of autoimmune diseases
- 专利标题（中）： TNF-A和TWEAK双重拮抗剂用于预防和治疗自身免疫性疾病
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申请号： US13635868申请日： 2011-03-18
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公开(公告)号： US08916525B2公开(公告)日： 2014-12-23
- 发明人: Young Woo Park , Ki Won Jo , Srok Ho Yoo , Jung Yu , Dong Jin Kim , Sun-Ha Yoon , Eun Jung Song , Eun Kyung Lee , Jin Mi Oh , Kyu Won Cho , Mi La Cho , Ho Youn Kim , Mi Kyung Park , Hye Jwa Oh , Jin Sil Park , Yun Ju Woo , Jae Kyeong Byun , Jun Geol Ryu
- 申请人： Young Woo Park , Ki Won Jo , Srok Ho Yoo , Jung Yu , Dong Jin Kim , Sun-Ha Yoon , Eun Jung Song , Eun Kyung Lee , Jin Mi Oh , Kyu Won Cho , Mi La Cho , Ho Youn Kim , Mi Kyung Park , Hye Jwa Oh , Jin Sil Park , Yun Ju Woo , Jae Kyeong Byun , Jun Geol Ryu
- 申请人地址： KR Taejeon-Si KR Seocho-Gu
- 专利权人： Korea Research Institute of Bioscience and Biotechnology,Industry-Academic Cooperation Foundation, The Catholic University of Korea
- 当前专利权人： Korea Research Institute of Bioscience and Biotechnology,Industry-Academic Cooperation Foundation, The Catholic University of Korea
- 当前专利权人地址： KR Taejeon-Si KR Seocho-Gu
- 代理机构： Lathrop & Gage LLP
- 优先权： KR10-2010-0024699 20100319
- 国际申请： PCT/KR2011/001900 WO 20110318
- 国际公布： WO2011/115456 WO 20110922
- 主分类号： A61K38/17
- IPC分类号： A61K38/17 ; A61P17/00 ; A61P19/02 ; A61P19/04 ; A61P21/00 ; A61P25/00 ; A61P3/10 ; A61P7/06 ; C07K14/525 ; C07K14/705
摘要：
The present invention relates to TNFR2-TWEAKR fusion protein, more precisely to TNFR2-TWEAKR fusion protein acting as a double-antagonist to TNF-α and TWEAK, known as major causes of autoimmune arthritis which is one of autoimmune diseases. When the composition comprising TNFR2-TWEAKR fusion protein was treated to Th17 cells, the secretion of the inflammatory cytokine IL-17 was reduced but the secretion of the anti-inflammatory cytokine IL-10 generated in Treg cells was increased. Such effect of TNFR2-TWEAKR fusion protein was far greater than that of a single protein such as TNFR2-Fc or TWEAK-Fc. The TNFR2-TWEAKR fusion protein of the present invention has not only excellent treatment effect on arthritis in CIA mouse model not also excellent treatment effect on autoimmune rheumatoid arthritis by increasing the expression of Treg, the immune suppressive cells. Therefore, the TNFR2-TWEAKR fusion protein of the present invention can be effectively used as an active ingredient for the composition for the prevention and treatment of autoimmune disease.
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