Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – C-o-group doai
Reexamination Certificate
2007-11-13
2007-11-13
Prouty, Rebecca E. (Department: 1652)
Drug, bio-affecting and body treating compositions
Designated organic active ingredient containing
C-o-group doai
C424S078020, C424S078080
Reexamination Certificate
active
10437427
ABSTRACT:
The invention relates to methods and materials involved in diagnosing and treating autoimmune conditions. In particular, the invention relates to methods and materials involved in diagnosing arthritis conditions that are accompanied by an NADPH oxidase deficiency, methods and materials involved in treating, preventing, or delaying the onset of arthritis conditions that are accompanied by an NADPH oxidase deficiency, and methods and materials involved in identifying agonists and antagonists of NADPH oxidase activity.
REFERENCES:
patent: 5128324 (1992-07-01), Walker et al.
patent: 5280048 (1994-01-01), Yamamoto et al.
patent: 19644422 (2000-06-01), None
patent: 2 285 047 (1995-06-01), None
patent: 1 827 623 (1993-07-01), None
patent: WO 94/20080 (1994-09-01), None
patent: WO 98/01120 (1998-01-01), None
patent: WO 98/02182 (1998-01-01), None
patent: WO 99/12539 (1999-03-01), None
patent: WO 99/46367 (1999-09-01), None
patent: WO 00/40241 (2000-07-01), None
patent: WO 01/42435 (2001-06-01), None
patent: WO 02/83058 (2002-10-01), None
patent: WO 02/83059 (2002-10-01), None
patent: WO 02/83122 (2002-10-01), None
van de Loo et al., NADPH oxidase deficiency caused deterioration of inflammation and connective tissue destruction in experimental arthritis. ACR Poster Session D, RA- Animal Models-1, Oct. 31, 2001, p. S230.
Mokgobu et al., The ketolide antimicrobial agent HMR-3004 inhibits neutrophil superoxide production by a membrane-stabilizing mechanism. Int. J. Immunopharmacol., 21: 365-377, 1999.
Schulz et al., “Perillic Acid Inhibits Ras/MAPkinase-Driven IL-2 Production in Human T Lymphocytes,”Biochem. Biophys. Res. Commun., 1997, 241:720-725.
Crandall et al., “Bb2Bb3Regulation of Murine Lyme Arthritis Is Distinct fromNcf1and Independent of the Phagocyte Nicotinamide Adenine Dinucleotide Phosphate Oxidase,”Am. J. Pathol., 2005, 167(3):775-785.
El Benna et al., “NADPH Oxidase Priming and p47phox Phosphorylation in Neutrophils from Synovial Fluid of Patients with Rheumatoid Arthritis and Spondylarthropathy,”Inflammation, 2002, 26(6):273-278.
Hultqvist and Holmdahl, “Ncf1(p47phox) polymorphism determines oxidative burst and the severity of arthritis in rats and mice,”Cell. Immunol., 2005, 233(2):97-101.
Hultqvist et al., “Enhanced autoimmunity, arthritis, and encephalomyelitis in mice with a reduced oxidative burst due to a mutation in theNcf1gene,”Proc. Natl. Acad. Sci. USA, 2004, 101(34):12646-12651.
Jackson et al., “T cells express a phagocyte-type NADPH oxidase that is activated after T cell receptor stimulation,”Nat. Immunol., 2004, 5(8):818-827.
Lloyds et al., “Tyrosine phosphorylation in neutrophils from synovial fluid of patients with rheumatoid arthritis,”Br. J. Rheumatol., 1996, 35(9):846-852.
Olofsson and Holmdahl, “Positional Cloning ofNcf1—a Piece in the Puzzle of Arthritis Genetics,”Scand. J. Immunol., 2003, 58(2):155-164.
Olofsson et al., “Inconsistent susceptibility to autoimmunity in inbred LEW rats is due to genetic crossbreeding involving segregation of the arthritis-regulating geneNcf1,” Genomics, 2004, 83(5):765-771.
Zhang et al., “The preventive effects of incomplete Freund's adjuvant and other vehicles on the development of adjuvant-induced arthritis in Lewis rats,”Immunology, 1999, 98(2):267-272.
Zheng et al., “Complete Freund's Adjuvant Suppresses the Development and Progression of Pristane-Induced Arthritis in Rats,”Clin. Immunol., 2002, 103(2):204-209.
De Mendez et al., “Specificity of p47phoxSH3 Domain Interactions in NADPH Oxidase Assembly and Activation,”Mol. Cell. Biol., 1997, 17(4):2177-2185.
Ellerman and Like, “A Major Histocompatibility Complex Class II Restriction for BioBreeding/Worcester Diabetes-inducing T Cells,” J. Exp. Med., 1995, 182:923-930.
Huang et al., “P47phox-deficient NADPH oxidase defect in neutrophils of diabetic mouse strains, C57BL/6J-m db/dbanddb/+,” J. Leuk. Biol., 2000, 67:210-215.
Joe et al., “Genetic dissection of collagen-induced arthritis in Chromosome 10 quantitative trait locus speed congenic rats: evidence for more than one regulatory locus and sex influences,”Immunogenetics, 2000, 51:930-944.
Miesel et al., “Assessment of collagen type II induced arthritis in mice by whole blood chemiluminescence,”Autoimmunity, 1994, 19:153-159.
Miesel et al., “Antiinflammatory effects of NADPH oxidase inhibitors,”Inflammation, 1995, 19(3):347-362.
Palicz et al., “Phosphatidic Acid and Diacylglycerol Directly Activate NADPH Oxidase by Interacting with Enzyme Components,”J. Biol. Chem., 2001, 276(5):3090-3097.
Repo et al., “Chemiluminescence responses and chemotaxis of monocytes from patients with early rheumatoid arthritis,”Scand. J. Rheumatol., 1996, 25:92-96.
Sambo et al., “Maintenance of Scleroderma Fibroblast Phenotype by the Constitutive Up-Regulation of Reactive Oxygen Species Generation Through the NADPH Oxidase Complex Pathway,”Arthritis&Rheumatism, 2001, 44(11):2653-2664.
Van de Loo et al., “NADPH Oxidase Deficiency Caused Deterioration of Inflammation and Connective Tissue Destruction in Experimental Arthritis,”Inflammation Research, 2000, 49(2):S90.
van der Veen et al., “Superoxide Prevents Nitric Oxide-Mediated Suppression of Helper T Lymphocytes: Decreased Autoimmune Encephalomyelitis in Nicotinamide Adenine Dinucleotide Phosphate Oxidase Knockout Mice,”J. Immunol., 2000, 164:5177-5183.
Vingsbo-Lundberg et al., “Genetic control of arthritis onset, severity and chronicity in a model for rheumatoid arthritis in rats,”Nature Genetics, 1998, 20:401-404.
Wilder et al., “Susceptibility to Autoimmune Disease and Drug Addiction in Inbred Rats. Are There Mechanistic Factors in Common Related to Abnormalities in H ypothalamic-Pituitary-Adrenal Axis and Stress Response Function?”Ann. N.Y. Acad. Sci., 2000, 917:784-796.
Brown, M. et al., “Mechanisms underlying mast cell influence on EAE disease course,”Molecular Immunology, 38:1373-1378 (2001).
Behi, M., “New insights into cell responses involved in experimental autoimmune encephalomyelitis and multiple sclerosis,”Immunology Letters, 96:11-26 (2005).
Craner, MJ., “Sodium channels contribute to microglia/macrophage activation and function in EAE and MS,”GLIA, 49:220-229 (2005).
Offner, H. et al., “Congruent effects of estrogen and T-cell receptor peptide therapy on regulatory T cells in EAE and MS,”International Reviews of Immunology, 24:447-477 (2005).
Pedotti, R. et al., “Involvement of both ‘allergic’ and ‘autoimmune’ mechanisms in EAE, MS and other autoimmune diseases,”Trends in Immunology, 24:479-484 (2003).
Steinman, L., “Optic neuritis, a new variant of experimental encephalomyelitis, a durable model for all seasons, now in its seventieth year,”J. Exp. Med., 197:1065-1071 (2003).
Ziemssen, T. et al., “The role of the humoral immune system in multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE),” Autoimmunity Reviews, 4:460-467 (2005).
OMIM website (Online Mendelian Inheritance in Man), MIM No. 126200, Multiple Sclerosis, Susceptibility to; MS, retrieved from http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=126200 on May 30, 2006, 30 pages.
Åkerström, “Immunological Analysis of α1-Microglobulin in Different Mammalian and Chicken Serum,”J. Biol. Chem., 1985, 260:4839-4844.
Casimir et al., “Autosomal recessive chronic granulomatous disease caused by deletion at a dinucleotide repeat,”Proc. Natl. Acad. Sci. USA, 1991, 88:2753-2757.
Dahlman et al., “Genome-Wide Linkage Analysis of Chronic Relapsing Experimental Automimmune Encephalomyelitis in the Rat Identifies a Major Susceptibility Locus on Chromosome 91,”J. Immunol.,
Holmdahl Rikard
Olofsson Peter
Arexis AB
Prouty Rebecca E.
Raghu Ganapathirama
LandOfFree
Autoimmune conditions and NADPH oxidase defects does not yet have a rating. At this time, there are no reviews or comments for this patent.
If you have personal experience with Autoimmune conditions and NADPH oxidase defects, we encourage you to share that experience with our LandOfFree.com community. Your opinion is very important and Autoimmune conditions and NADPH oxidase defects will most certainly appreciate the feedback.
Profile ID: LFUS-PAI-O-3834736