Pharmaceutical Compositions for Preventing or Treating Th1-Mediated Immune Diseases
[Problems] The present invention provides a pharmaceutical composition for preventing or treating Th1-mediated immune diseases. [Means for Solving] There is obtained a pharmaceutical composition provided for prevention or treatment of Th1-mediated immune diseases, which comprises as an active ingredient a substance capable of acting on the NP receptor GC-A expressed on dendritic cells to enhance cGMP production and thereby driving T cells to differentiate into Th2-type cells by regulating cytokine production from dendritic cells.
1 . A pharmaceutical composition for preventing or treating a Th1-mediated immune disease, which comprises as an active ingredient a substance capable of acting on the natriuretic peptide receptor guanylyl cyclase A to enhance the production of cyclic guanosine monophosphate in an amount effective to prevent or treat a Th1-mediated immune disease.
2 . The pharmaceutical composition according to claim 1 , wherein the Th1-mediated immune disease is a disease due to graft rejection following transplantation, graft-versus-host disease caused by bone marrow transplantation, or an autoimmune disease.
3 . The pharmaceutical composition according to claim 2 , wherein the autoimmune disease is autoimmune hepatitis, chronic rheumatoid arthritis, insulin-dependent diabetes mellitus, ulcerative colitis, Crohn's disease, multiple sclerosis, autoimmune myocarditis, psoriasis, scleroderma, myasthenia gravis, multiple myositis/dermatomyositis, Hashimoto's disease, autoimmune hypocytosis, pure red cell aplasia, aplastic anemia, Sjogren's syndrome, vasculitis syndrome, or systemic lupus erythematosus.
4 . The pharmaceutical composition according to claim 3 , wherein the autoimmune disease is Crohn's disease or multiple sclerosis.
5 . The pharmaceutical composition according to claim 1 , wherein the substance capable of acting on the natriuretic peptide receptor guanylyl cyclase A to enhance the production of cyclic guanosine monophosphate is a natriuretic peptide.
6 . The pharmaceutical composition according to claim 5 , wherein the natriuretic peptide is atrial natriuretic peptide or brain natriuretic peptide.
7 . The pharmaceutical composition according to claim 6 , wherein the atrial natriuretic peptide is of human origin.
8 . A method for treating a Th1-mediated immune disease, which comprises administering a substance capable of acting on the natriuretic peptide receptor guanylyl cyclase A to enhance the production of cyclic guanosine monophosphate.
9 . The method according to claim 8 , wherein the Th1-mediated immune disease is a disease due to graft rejection following transplantation, graft-versus-host disease caused by bone marrow transplantation, or an autoimmune disease.
10 . The method according to claim 9 , wherein the autoimmune disease is autoimmune hepatitis, chronic rheumatoid arthritis, insulin-dependent diabetes mellitus, ulcerative colitis, Crohn's disease, multiple sclerosis, autoimmune myocarditis, psoriasis, scleroderma, myasthenia gravis, multiple myositis/dermatomyositis, Hashimoto's disease, autoimmune hypocytosis, pure red cell aplasia, aplastic anemia, Sjogren's syndrome, vasculitis syndrome, or systemic lupus erythematosus.
11 . The method according to claim 10 , wherein the autoimmune disease is Crohn's disease or multiple sclerosis.
12 . The method according to claim 8 , wherein the substance capable of acting on the natriuretic peptide receptor guanylyl cyclase A to enhance the production of cyclic guanosine monophosphate is a natriuretic peptide.
13 . The method according to claim 12 , wherein the natriuretic peptide is atrial natriuretic peptide or brain natriuretic peptide.
14 . The method according to claim 13 , wherein the atrial natriuretic peptide is of human origin.
15 . A method of manufacturing a pharmaceutical composition for preventing or treating a Th1-mediated immune disease comprising admixing a substance capable of acting on the natriuretic peptide receptor guanylyl cyclase A to enhance the production of cyclic guanosine monophosphate with a pharmacologically acceptable carrier, excipient or diluent.
16 . The method according to claim 15 , wherein the Th1-mediated immune disease is a disease due to graft rejection following transplantation, graft-versus-host disease caused by bone marrow transplantation, or an autoimmune disease.
17 . The method according to claim 16 , wherein the autoimmune disease is autoimmune hepatitis, chronic rheumatoid arthritis, insulin-dependent diabetes mellitus, ulcerative colitis, Crohn's disease, multiple sclerosis, autoimmune myocarditis, psoriasis, scleroderma, myasthenia gravis, multiple myositis/dermatomyositis, Hashimoto's disease, autoimmune hypocytosis, pure red cell aplasia, aplastic anemia, Sjogren's syndrome, vasculitis syndrome, or systemic lupus erythematosus.
18 . The method according to claim 17 , wherein the autoimmune disease is Crohn's disease or multiple sclerosis.
19 . The method according to claim 15 , wherein the substance capable of acting on the natriuretic peptide receptor guanylyl cyclase A to enhance the production of cyclic guanosine monophosphate is a natriuretic peptide.
20 . The method according to claim 19 , wherein the natriuretic peptide is atrial natriuretic peptide or brain natriuretic peptide.
21 . The method according to claim 20 , wherein the atrial natriuretic peptide is of human origin.
22 . A method for regulating the Th1/Th2 balance in the immune system, which comprises treating dendritic cells with a substance capable of acting on the natriuretic peptide receptor guanylyl cyclase A to enhance the production of cyclic guanosine monophosphate, and thereby polarizing T cells toward Th2-promoting phenotype.
23 . The method according to claim 22 , wherein the substance capable of acting on the natriuretic peptide receptor guanylyl cyclase A to enhance the production of cyclic guanosine monophosphate is a natriuretic peptide.
24 . The method according to claim 23 , wherein the natriuretic peptide is atrial natriuretic peptide or brain natriuretic peptide.
25 . The method according to claim 24 , wherein the atrial natriuretic peptide is of human origin.