Model animal with favorite onset or rheumatoid arthritis

Multicellular living organisms and unmodified parts thereof and – Nonhuman animal – Transgenic nonhuman animal

Reexamination Certificate

Rate now

  [ 0.00 ] – not rated yet Voters 0   Comments 0

Details

C800S021000

Reexamination Certificate

active

07081562

ABSTRACT:
The present invention provides a model animal with favorite onset of rheumatoid arthritis wherein the severity of arthritis reaches the maximum level and its onset ratio is a hundred percent, and a screening method of a remedy for rheumatoid arthritis by using the model animal. A mouse whose function of immunoglobulin Fcγ receptor IIB gene is deficient on its chromosome and a wild-type collagen-induced arthritis-susceptible DBA/1J mouse are backcrossed six times or more, and a model mouse with favorite onset of rheumatoid arthritis is constructed. This model mouse with favorite onset of rheumatoid arthritis is immunized with bovine joint-origin type II collagen to develop collagen-induced arthritis.

REFERENCES:
Kleinau et al. (May 1, 2000) Induction and suppression of collagen-induced arthritis is dependent on distinct Fc(gamma) receptors. Journal of Experimental Medicine 191(9): 1611-1616.
Campbell and Wilmut (1997) Totipotency or multipotentiality of cultured cells: Applications and progress. Theriogenology 47: 63-72.
Doetschman, T. (1999) Interpretation of phenotype in genetically engineered mice. Laboratory Animal Science 49(2): 137-143.
Donehower et al. (1995) Effects of genetic background on tumorigenesis in p53-deficient mice. Molecular Carcinogenesis 14: 16-22.
Jacks et al. (1992) Effects of an Rb mutation in the mouse. Nature 359: 295-300.
Jaenisch et al. (1988) Transgenic Animals. Science 240: 1468-1474.
Kuehn et al. (1987) A potential animal model for Lesch-Nyhan syndrome through introduction of HPRT mutations into mice. Nature 326: 295-298.
Moens et al. (1993) Defects in heart and lung development in compound heterozygotes for two different targeted mutations at the N-myc locus. Development 119: 485-499.
Mullins et al. (1996) Transgenesis in the rat and larger mammals. J. Clin. Invest. 97(7): 1557-1560.
Petridou et al. (2003) Heterogeneous inducible mammary-specific expression of JAB/SOCS1 in lactating transgenic mice is associated with no obvious phenotype, even at the cellular level. Transgenic Research 12: 693-706.
Sigmund, CD (2000) Viewpoint: Are studies in genetically altered mice out of control? Arterioscler. Thromb. Vasc. Biol. 20: 1425-1429.
Sandra Kleinau, et al., “Induction and Suppression of Collagen-induced Arthritis Is Dependent on Distinct Fcβ Receptors”, Journal of Experimental Medicine, May 1, 2000, pp. 1611-1616, vol. 191, No. 9.
Takae Yuasa, et al., “Deletion of Fcβ Receptor IIB Renders H-2bMice Susceptible to Collagen-induced Arthritis”, Journal of Experimental Medicine, Jan. 4, 1999, pp. 187-194, vol. 189, No. 1.
Toshiyuki Takai, et al., “Augmented humoral and anaphylactic responses in FcγRII-deficient mice”, Nature, Jan. 1996, pp. 346-349, vol. 379, No. 25.
Linda K. Myers, et al., “Collagen-Induced Arthritis, An Animal Model Of Autoimmunity”, Life Science, 1997, pp. 1861-1874, vol. 61, NO. 19.
Paul H. Wooley, et al., “Variations in Immunogenetic Regulation Provide Evidence for Multiple Arthritogenic Epitopes on the Collagen Molecule1”, The Journal of Immunology, Oct. 1985, pp. 2443-2451, vol. 135, No. 4.
Raphael Clynes, et al., “Modulation of Immune Complex-induced InflammationIn vivoby the Coordinate Expression of Activation and Inhibitory Fc Receptors”, Journal of Experimental Medicine, Jan. 4, 1999, pp. 179-185, vol. 189, No. 1.
Paul H. Wooley, et al., “Major Histocompatibility Complex (1 Region) Linkage and Antibody Correlates”, Journal of Experimental Medicine, Sep. 1981, pp. 688-700, vol. 154, No. 3.
Mikael C.I. Karlsson, et al., “Efficient IgG-mediated suppression of primary antibody responses in Fcγ receptor-deficient mice”, Proc. Natl. Acad. Sci., Mar. 2, 1999, pp. 2244-2249, vol. 96.
Sara Wernersson, et al., “IgG-Mediated Enhancement of Antibody Responses Is low in Fc Receptor γ Chain-Deficient Mice and Increased in FcγRII-Deficient Mice1”, The Journal of Immunology, Jul. 15, 1999, pp. 618-622, vol. 163, No. 2.
Sebastian Amigorena, et al., “Cytoplasmic Domain Heterogeneity and Functions of IgG Fc Receptors in B Lymphocytes”, Science, Jun. 26, 1992, pp. 1808-1812, vol. 256.
Wolf H. Fridman, et al., “Structural Bases of Fcγ Receptor Functions”, Immunological Reviews, 1992, pp. 49-76, No. 125.

LandOfFree

Say what you really think

Search LandOfFree.com for the USA inventors and patents. Rate them and share your experience with other people.

Rating

Model animal with favorite onset or rheumatoid arthritis does not yet have a rating. At this time, there are no reviews or comments for this patent.

If you have personal experience with Model animal with favorite onset or rheumatoid arthritis, we encourage you to share that experience with our LandOfFree.com community. Your opinion is very important and Model animal with favorite onset or rheumatoid arthritis will most certainly appreciate the feedback.

Rate now

     

Profile ID: LFUS-PAI-O-3601411

  Search
All data on this website is collected from public sources. Our data reflects the most accurate information available at the time of publication.