Korea Research Institute of Bioscience and Biotechnology

Industry-Academic Cooperation Foundation, the Catholic University of Korea

Jin Sil Park

Young Woo Park

Jung Jae Yu

Mi Kyung Park

Mi La Cho

Ho Youn Kim

Ki Won Jo

Jun Geol Ryu

Jae Kyeong Byun

Yun Ju Woo

Sun-Ha Yoon

Eun Jung Song

Srok Ho Yoo

Hye Jwa Oh

Jong-Ho Lee

Eun Kyung Lee

Ji Hyun Park

Dong Jin Kim

Min Ji Seo

Kyu Won Cho

Jin Mi Oh

Sun Jung Cho

The present invention relates to TNFR2-IL21R fusion protein acting as a double-antagonist to TNF-alpha (&#x3b1;) and IL-21. The composition containing the double antagonist to TNF-&#x3b1; and Il-21 (TNFR2-IL21R fusion protein), known as major causes of autoimmune rheumatoid arthritis, one of autoimmune diseases, can reduce the secretion of inflammatory cytokine, increase the secretion of anti-inflammatory cytokine, and suppress the differentiation of osteoclasts better than single proteins such as TNFR2-Fc and IL21R-Fc. The TNFR2-IL21R 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-IL21R 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.

Dual antagonist for TNF-&#x3b1; and IL-21 for preventing and treating autoimmune diseases

The present invention relates to TNFR2-TWEAKR fusion protein, more precisely to TNFR2-TWEAKR fusion protein acting as a double-antagonist to TNF-&#x3b1; 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.

TNF-A and TWEAK dual antagonist for the prophylaxis and treatment of autoimmune diseases

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Seoul, South Korea

Jin Sil Park