Drug – bio-affecting and body treating compositions – Extract or material containing or obtained from an alga as...
Reexamination Certificate
2002-03-28
2004-08-10
Prats, Francisco (Department: 1654)
Drug, bio-affecting and body treating compositions
Extract or material containing or obtained from an alga as...
C514S725000
Reexamination Certificate
active
06773708
ABSTRACT:
The present invention relates to the use and method of treatment concerning utilization of xanthophylls, e.g. astaxantin for suppression of excessive Th1 cell mediated immune responses and stimulation of Th2 cell mediated immune responses in a patient during ongoing infection and/or inflammation in said patient.
BACKGROUND OF THE INVENTION
CD4 T lymphocytes can be subdivided into two major subsets—Th1 cells and Th2 cells. These cells release different sets of cytokines that define their distinct actions in immunity. Th1 cells secrete interferon-gamma (IFN-&ggr;) and are mainly involved in activating macrophages and CD8+ cytotoxic T-lymphocytes. Th2 cells secrete the interleukins Il-4, Il-5 and Il-10 and are mainly involved in stimulating B cells to produce antibodies.
There is a balance between the activities of the Th1 and Th2 cells in a normal human body. An excess of Th1 cell activity may be the result of an autoimmune disease, or the result of an ongoing infection. In the normal case, the Th1 cell activity diminishes when the physiological need thereof is reduced. An excess activity is thus seen when the normal reduced level of Th1 cell activity is not achieved as a response to the diminishing presence of the agent that induced the reaction, e.g. the starting point of an autoimmune disease.
Immune modulation aims at altering the balance between different subsets of responding T cells so that damaging responses are suppressed In many cases autoimmune diseases and intracellular infections are associated with the activation of Th1 cells, which activate macrophages and drive an inflammatory immune response. The drugs currently used to suppress the immune system can be divided into three categories:
1) Powerful anti-inflammatory drugs of the corticosteroid family such as prednisone. Glucocorticoids influence virtually every cellular and humoral mechanism related to inflammation and immune response. However, there are also many adverse effects, including fluid retention, weight gain, diabetes, bone mineral loss and thinning of the skin.
2) Cytotoxic drugs such as azthioprine and cyclophosphamide. Cytotoxic drugs cause immunosuppression by killing dividing cells and they have serious side-effects. The use of these compounds is limited due to a range of toxic effects on tissues that have continuous cell dividing, such as the bone marrow.
3) Cyclosporin A, tacromycin and rapamycin are powerful immunosuppressive agents that interfere with T-cell signaling.
All of these drugs are very broad in their action and inhibit protective functions of the immune system as well as pathological responses that cause tissue injury. Opportunistic infection is therefore a common complication of immune suppressive drugs.
It would be desirable to have an immunosuppressive agent that targets the specific part of the immune response that causes tissue injury. In particular, it would be desirable to obtain a medicament for suppression of harmful, i.e. excessive, Th1 cell mediated immune responses and simulation of Th2 cell mediated immune responses in a patient during ongoing infection and/or inflammation in said patient.
REFERENCES:
patent: 5744502 (1998-04-01), Lignell et al.
patent: 5811446 (1998-09-01), Thomas
patent: 5886053 (1999-03-01), Schmutzler et al.
STN International, File CA, Chemical abstracts, vol. 119, No. 11, Sep. 13, 1993, (Columbus, Ohio, US), Date, Yukio et al: “Lipid peroxide-lowering compositions” & JP, A2, 05124958, 19930521, Heisei.
Nutr Cancer, vol. 26, 1996, Harumi Jyonouchi et al., “Effects of Various Carotenoids on Cloned, Effector-Stage T-Helper Cell Activity” p. 313-324.
Clinical and Diagnostic Laboratory Immunology, vol. 6, No. 3, May 1999, Sami T. Azar et al., “Type 1 (Insulin-Dependent) Diabetes is a Th1 and Th2-Mediated Autoimmune Disease”, p. 306-310.
Böttiger Per
Lignell Åke
AstaReal AB
Bacon & Thomas
Coe Susan D.
Prats Francisco
LandOfFree
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