US2005158302A1PendingUtilityA1

Methods for diagnosing and treating autoimmune disease

Assignee: GEN HOSPITAL CORPPriority: Feb 27, 1998Filed: Feb 10, 2004Published: Jul 21, 2005
Est. expiryFeb 27, 2018(expired)· nominal 20-yr term from priority
G01N 33/564C07K 14/4702A61K 38/00G01N 2800/042C07K 14/4703G01N 2333/9121A61P 37/06G01N 2333/96425C12Q 1/37C12N 9/6421C12N 9/1205G01N 2500/04A61K 48/00
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Claims

Abstract

The invention provides a method of activating NFκB activity in a mammal afflicted with an autoimmune disease in which a reduction in NFκB activity is observed, comprising administering to a mammal suffering from the autoimmune disease a therapeutically effective amount of a polypeptide which activates NFκB, so as to treat the autoimmune disease in the mammal.

Claims

exact text as granted — not AI-modified
1 - 75 . (canceled)  
     
     
         76 . A method of treating a mammal having, or predisposed to having, an autoimmune disease, said method comprising administering to said mammal a therapeutically effective amount of a substance that stimulates a signaling pathway that activates NFκB.  
     
     
         77 . The method of  claim 76 , wherein said substance is TNF-α.  
     
     
         78 . The method of  claim 77 , wherein said substance is an antibody, an antisense RNA molecule, or a ribozyme directed against IκB or one of the 240 kD or 200 kD human erythrocyte derived proteasome inhibitors.  
     
     
         79 . The method of  claim 76 , wherein said mammal is a human.  
     
     
         80 . The method of  claim 76 , wherein said disease is diabetes, rheumatoid arthritis, multiple sclerosis, lupus erythematosis, myasthenia gravis, scleroderma, Crohn's disease, ulcerative colitis, Hashimoto's disease, Graves' disease, Sjögren's syndrome, polyendocrine failure, vitiligo, peripheral neuropathy, graft-versus-host disease, autoimmnune polyglandular syndrome type I, acute glomerulonephritis, Addison's disease, adult-onset idiopathic hypoparathyroidism (AOIH), alopecia totalis, amyotrophic lateral sclerosis, ankylosing spondylitis, autoimmune aplastic anemia, autoimmune hemolytic anemia, Behcet's disease, Celiac disease, chronic active hepatitis, CREST syndrome, dermatomyositis, dilated cardiomyopathy, eosinophilia-myalgia syndrome, epidermolisis bullosa acquisita (EBA), giant cell arteritis, Goodpasture's syndrome, Guillain-Barrë syndrome, hemochromatosis, Henoch-Schönlein purpura, idiopathic IgA nephropathy, insulin-dependent diabetes mellitus (IDDM), juvenile rheumatoid arthritis, Lambert-Eaton syndrome, linear IgA dermatosis, myocarditis, narcolepsy, necrotizing vasculitis, neonatal lupus syndrome (NLE), nephrotic syndrome, pemphigoid, pemphigus, polymyositis, primary sclerosing cholangitis, psoriasis, rapidly-progressive glomerulonephritis (RPGN), Reiter's syndrome, stiff-man syndrome, or thyroiditis.  
     
     
         81 . A method of treating a mammal having, or predisposed to having, an autoimmune disease, said method comprising the steps of: 
 a. measuring the activity of NFκB in said mammal; and    b. if the activity of step (a) is less than a basal state level, administering to said mammal a therapeutically effective amount of a substance that stimulates a signaling pathway that activates NFκB.    
     
     
         82 . The method of  claim 81 , wherein said substance is TNF-α, or an antibody, antisense RNA molecule, or ribozyme directed against IκB or one of the 240 kD or 200 kD human erythrocyte derived proteasome inhibitors.

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