Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Peptide containing doai
Patent
1994-10-20
1997-07-15
Walsh, Stephen
Drug, bio-affecting and body treating compositions
Designated organic active ingredient containing
Peptide containing doai
A61K 3817
Patent
active
056483325
DESCRIPTION:
BRIEF SUMMARY
BACKGROUND OF THE INVENTION
1. Field of the Invention
This invention relates to a prophylactic and therapeutic agent for autoimmune diseases. More particularly, it is concerned with a prophylactic and therapeutic agent for autoimmune diseases generated to a wide variety of autoantigens which comprises as an active ingredient of a soluble T-cell receptor .alpha.-chain produced by the said suppressor T-cell. 2. Description of the Prior Art
Autoimmune diseases are meant to be a generic term for the immune diseases which would cause various disturbances by forming autoantibodies and cytotoxic T-cells to the antigen derived from autologous tissues. The autoimmune diseases may include non-organ specific diseases such as systemic lupus erythematosus, chronic rheumatoid arthritis, systemic sclerosis, dermatomyositis/multiple myositis, Sjogren's syndrome and others; organ specific diseases such as diabetes, Hashimoto's thyroiditis, Graves' disease, multiple sclerosis, idiopathic Addison's disease, myasthenia gravis, pernicious anemia, and others; as well as mixed diseases such as primary biliary cirrhosis, chronic active hepatitis and others, and the total number of those patients suffering from such diseases including latent patients has been enormous.
The therapy hitherto practically applied for the treatment of such autoimmune diseases may include administration of such therapeutic agents as corticosteroids, cyclosporin A, cyclophosphamide, azathiopurine, methotrexate and the like, expecting their immunosuppressive activity; or X-ray irradiation, thymectomy and others; or administration of interferon, .gamma.-globulin, antibody to lymphoid cell surface marker, gold preparations, D-penicillamine and the like, expecting their immunoregulating activity.
Many of such immunosuppressants could damage the DNA or RNA in various cells including immunocompetent cells and, accordingly, there would be developed severe side-effects if one may use them in an erroneous manner. Moreover, administration to pregnant women would cause birth of malformed babies and it has been also pointed out that there may be strengthened a risk of opportunistic infection because of widespread immunosuppression induced. On the other hand, a detailed mechanism of action in an immune regulator has not yet been known so that it would be difficult to predict a therapeutic effect exactly. And further, it has been pointed out that there would be a high risk of side-effects because of a wide variety of cell groups to be influenced.
As discussed above, there have been found many unsatisfactory points in the existing, therapies against autoimmune diseases. Also, there have been found many unsolved points in the mechanism of onset of autoimmune diseases. It has been strong grounds to hinder development of the therapeutic agent capable of acting specifically on abnormal portions only in the immune system, inducing autoimmune diseases.
BRIEF DESCRIPTION OF THE DRAWINGS
FIG. 1 shows the results wherein the expression levels of the mRNA encoding the T-cell receptor .alpha.chain, V.alpha.14J.alpha.281 in spleen lymphocytes of NOD mice were determined every week of age. In this Figure, the closed circles show changes in the mRNA corresponding to the present V.alpha.14J.alpha.281C.alpha., while the open circles and open squares show changes in the mRNA corresponding to VxJ.alpha.281C.alpha. and V.alpha.14JxC.alpha. employed as the control groups, respectively.
FIG. 2 shows the construction of the expression vector plasmid of the gene encoding the chimeric protein of a T-cell receptor .alpha.-chain and an immunoglobulin constant region.
FIG. 3 shows the inhibition of the antibody production to the KLH antigen of the mice pre-treated with the anti-V.alpha.14 monoclonal antibody. In this Figure, the closed circles show the anti-V.alpha.14 monoclonal antibody-administered group, while the open circles show the control group.
FIG. 4 shows the inhibition of the antibody production to the DNP antigen of the mice pre-treated with the anti-V.alpha.14 monoclonal antibo
REFERENCES:
Davies et al. (1991). New England Journal of Medicine 325, 238-244.
Yamamura et al. (1994). International Immunology 6, 947-954.
Ito et al. (1991). International Immunology 3, 991-995.
Vandenbark et al. (1989). Nature 341, 541-544.
Koseki et al. (1992). Int'l. Archives of Allergy and Immunology 99, 416-418 .
Taniguchi Masaru
Watanabe Hiroshi
Yamagata Nobuyuki
Brown Karen E.
Hoechst Japan Limited
Walsh Stephen
LandOfFree
Method of treating diabetes mellitus using variable .alpha. doma does not yet have a rating. At this time, there are no reviews or comments for this patent.
If you have personal experience with Method of treating diabetes mellitus using variable .alpha. doma, we encourage you to share that experience with our LandOfFree.com community. Your opinion is very important and Method of treating diabetes mellitus using variable .alpha. doma will most certainly appreciate the feedback.
Profile ID: LFUS-PAI-O-1492362