Abstract: The present disclosure relates to a method for inhibiting a STAT3 activity comprising administering SSu72 protein.

Abstract: The present disclosure relates to a method for inhibiting a STAT3 activity, and a method for treating inflammatory bowel disease (IBD).

Abstract: The present disclosure relates to a method of preventing rheumatoid arthritis comprising administering a polynucleotide encoding Ssu72.

Abstract: The present invention relates to a novel use of a thiourea derivative and, more specifically, to a pharmaceutical composition for preventing or treating autoimmune diseases comprising a thiourea derivative as an active ingredient. The thiourea derivative according to the present invention can inhibit the transcription of inflammatory genes such as TNF-?, IL-1?, NOS2 and IL-6, and also can inhibit the activity or production of Th17 and increase the activity or production of a regulatory T cell (Treg). Thus, it is expected that the thiourea derivative may be usefully used in a pharmaceutical composition, a health food composition, etc. for the prevention, improvement or treatment of various autoimmune diseases including rheumatoid arthritis.

Abstract: The present disclosure relates to a composition for preventing or treating an autoimmune disease, in which the composition includes Ssu72 as an active ingredient. According to the present invention, Ssu72 has an effect of effectively inhibiting STAT3 activity, thereby effectively preventing and treating, ultimately, an immune disease, and preferably, STAT3-mediated diseases through an action capable of inhibiting the expression of inflammatory cytokines when Ssu72 is overexpressed and simultaneously promoting the expression of IL-4 and IL-10, which are factors associated with immunoregulatory T cells.

Abstract: The present invention relates to a composition for treating or preventing bone diseases comprising halofuginone as an active ingredient and, more specifically, to a composition for treating or preventing bone diseases, comprising, as an active ingredient, halofuginone having an osteoclast differentiation inhibitory efficacy and an osteoblast differentiation stimulatory activity. The composition for treating or preventing bone diseases, comprising halofuginone as an active ingredient, according to the present invention, reduces the expression of Th17 cells and increases the expression of Treg cells, thereby representing an effect of inhibiting osteoclast differentiation and being capable of also effectively inhibiting bone resorption by osteoclasts. Furthermore, the composition of the present invention will be able to be usefully utilized as a use for the treatment or prevention of bone diseases by being able to promote the differentiation and activity of osteoblast.

Abstract: The present invention relates to TNFR2-IL21R fusion protein acting as a double-antagonist to TNF-alpha (?) and IL-21. The composition containing the double antagonist to TNF-? 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.

Abstract: The present invention relates to TNFR2-TWEAKR fusion protein, more precisely to TNFR2-TWEAKR fusion protein acting as a double-antagonist to TNF-? 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.

Abstract: The present invention relates to TNFR2-IL21R fusion protein acting as a double-antagonist to TNF-alpha (?) and IL-21. The composition containing the double antagonist to TNF-? 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.

Abstract: The present invention relates to TNFR2-TWEAKR fusion protein, more precisely to TNFR2-TWEAKR fusion protein acting as a double-antagonist to TNF-? 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.

Abstract: The present invention provides an improved process for preparing a Vitis vinifera pip extract. And also, the present invention provides a pharmaceutical composition for preventing or treating rheumatoid arthritis including the Vitis vinifera pip extract as an active ingredient.