WO2003086310A2 - Prevention of brain inflammation as a result of induced autoimmune response - Google Patents
Prevention of brain inflammation as a result of induced autoimmune response Download PDFInfo
- Publication number
- WO2003086310A2 WO2003086310A2 PCT/US2003/011316 US0311316W WO03086310A2 WO 2003086310 A2 WO2003086310 A2 WO 2003086310A2 US 0311316 W US0311316 W US 0311316W WO 03086310 A2 WO03086310 A2 WO 03086310A2
- Authority
- WO
- WIPO (PCT)
- Prior art keywords
- amyloid
- antibodies
- accordance
- disease
- receptors
- Prior art date
Links
Classifications
-
- C—CHEMISTRY; METALLURGY
- C07—ORGANIC CHEMISTRY
- C07K—PEPTIDES
- C07K16/00—Immunoglobulins [IGs], e.g. monoclonal or polyclonal antibodies
- C07K16/18—Immunoglobulins [IGs], e.g. monoclonal or polyclonal antibodies against material from animals or humans
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
- A61K39/00—Medicinal preparations containing antigens or antibodies
- A61K2039/505—Medicinal preparations containing antigens or antibodies comprising antibodies
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
- A61K39/00—Medicinal preparations containing antigens or antibodies
- A61K2039/545—Medicinal preparations containing antigens or antibodies characterised by the dose, timing or administration schedule
-
- C—CHEMISTRY; METALLURGY
- C07—ORGANIC CHEMISTRY
- C07K—PEPTIDES
- C07K2317/00—Immunoglobulins specific features
- C07K2317/50—Immunoglobulins specific features characterized by immunoglobulin fragments
-
- C—CHEMISTRY; METALLURGY
- C07—ORGANIC CHEMISTRY
- C07K—PEPTIDES
- C07K2317/00—Immunoglobulins specific features
- C07K2317/50—Immunoglobulins specific features characterized by immunoglobulin fragments
- C07K2317/54—F(ab')2
-
- C—CHEMISTRY; METALLURGY
- C07—ORGANIC CHEMISTRY
- C07K—PEPTIDES
- C07K2317/00—Immunoglobulins specific features
- C07K2317/50—Immunoglobulins specific features characterized by immunoglobulin fragments
- C07K2317/55—Fab or Fab'
-
- C—CHEMISTRY; METALLURGY
- C07—ORGANIC CHEMISTRY
- C07K—PEPTIDES
- C07K2317/00—Immunoglobulins specific features
- C07K2317/60—Immunoglobulins specific features characterized by non-natural combinations of immunoglobulin fragments
- C07K2317/62—Immunoglobulins specific features characterized by non-natural combinations of immunoglobulin fragments comprising only variable region components
- C07K2317/622—Single chain antibody (scFv)
Definitions
- the present invention is directed to methods for reducing risk of inflammation as a result of induced autoimmune response and particularly as a result of immunotherapy of diseases characterized by amyloid aggregation.
- a peptide which may be an entire amyloid peptide or a portion thereof, is administered in order to raise antibodies in vivo, which antibodies will bind to the soluble and/or the aggregated amyloid.
- - Passive vaccination involves administering antibodies specific to the amyloid peptide directly. These procedures are preferably used for the treatment of Alzheimer's disease by diminishing the amyloid plaque or slowing the rate of deposition of such plaque.
- Antibody-antigen complexes initiate the inflammatory response and are central to the pathogenesis of tissue injury.
- the immune complex triggers inflammation, which is initialized by cell bound Fc receptors, and is then amplified by cellular- mediators and activated complement.
- the accepted model of inflammation is one in which antibodies bind their antigen, forming immune complex, which in turn binds and activates the complement by means of the "classical pathway" (Clynes et al, 1995) .
- FcR immunoglobulin
- the diversity of these receptors is reflected in a wide variety of biological responses immediately upon their binding of IgG-antigen complexes, including phagocytosis, endocytosis, antibody-dependent cell-mediated cytotoxicity (ADCC) , release of inflammatory mediators and regeneration of B-cell function (Clynes et al, 1995) .
- the present invention solves the problem of increased risk of brain inflammation as a result of induced autoimmune response by eliminating the inflammation pathway initiated by binding of an immune complex to an Fc receptor.
- the present invention is based on the realization that the brain inflammation that caused the cessation of the clinical trials for AN-1792 was most likely caused by the inflammatory reaction initiated by binding of the immune complex to Fc receptors.
- This immune reaction could be stopped before it begins by one of two techniques in accordance with the present invention.
- the first such technique is to block the Fc receptors prior to commencing the immunotherapy.
- the preferred way to do this is to administer a large dose of IVIg, i.e., human intact intravenously administered immunoglobulin.
- Intravenous immunoglobulins have become an established component of immunomodulatory therapy in neurological autoimmune diseases, including inflammatory diseases of the central nervous system (CNS) (van der Meche and van Doom, 1997/ Dalakis, 1999; Stangel et al, 1999) .
- This embodiment of the present invention is based on the realization that IVIg can be used as a preventive step prior to immunotherapy designed to cause antibodies against amyloid- ⁇ to come into contact with aggregated or soluble amyloid- ⁇ in vivo, regardless of whether the antibodies are directly administered or generated in vivo by administering an antigenic peptide, such as an amyloid peptide.
- the second method to avoid binding of the immune complex to Fc receptors is to use antibodies that are devoid of Fc regions.
- antibodies devoid of Fc regions include Fab, F(ab) 2 and/or scFv antibodies.
- Such antibodies will still bind to the amyloid or amyloid plaque, but the immune complexes will not start the inflammation sequence because they will not bind to Fc receptors.
- Alzheimer's disease Parkinson's disease, multiple sclerosis
- glia especially microglia, become activated (a process termed reactive gliosis) following an initial wave of neuronal death resulting from traumatic injury, exposure to neurotoxins, and ischemia in the brain.
- Activated microglia produce a variety of proinflammatory and cytotoxic factors including cytokines.
- Microglia are very sensitive to changes in the CNS microenvironment and rapidly become activated in virtually all conditions that disrupt normal neuronal functions.
- microglia Upon activation, microglia secrete a range of immune regulatory peptides as cytokines and non-specific inflammatory mediators, e.g., nitric oxide, and become phagocytic, thus representing the latent scavenger cells of the CNS (Liu et al, 2001) .
- IVIg intravenous immunoglobulins
- MS multiple sclerosis
- ADAM acute demyelinating encephalomyelitis
- IVIg intravenous immunoglobulins
- Fc receptor-mediated phagocytosis was inhibited by IVIg, presumably by blockage of the Fc receptor (Stangel et al, 2001) .
- IVIg in addition to known effects on the peripheral immune system, may also be used to modulate the local immune reaction in CNS inflammatory disease.
- Phages as a delivery system of scFv and Fab are able to remove the plaque via efflux from brain-blood or other peripheral membranes.
- a phage delivery system, or any other carrier for the antibody which potentiates efflux of the immune system of the immune complex is a preferred embodiment of the present invention.
- the IVIg injection method for blocking the majority of Fc receptors in microglia, prior to the i.p or i.n. injection of whole antibodies should be undertaken in order to avoid over-activation of microglia.
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- Chemical & Material Sciences (AREA)
- Organic Chemistry (AREA)
- Health & Medical Sciences (AREA)
- General Health & Medical Sciences (AREA)
- Biochemistry (AREA)
- Biophysics (AREA)
- Life Sciences & Earth Sciences (AREA)
- Genetics & Genomics (AREA)
- Medicinal Chemistry (AREA)
- Molecular Biology (AREA)
- Proteomics, Peptides & Aminoacids (AREA)
- Immunology (AREA)
- Medicines Containing Antibodies Or Antigens For Use As Internal Diagnostic Agents (AREA)
- Peptides Or Proteins (AREA)
- Medicines That Contain Protein Lipid Enzymes And Other Medicines (AREA)
Abstract
Description
Claims
Priority Applications (3)
Application Number | Priority Date | Filing Date | Title |
---|---|---|---|
AU2003226356A AU2003226356A1 (en) | 2002-04-12 | 2003-04-14 | Prevention of brain inflammation as a result of induced autoimmune response |
US10/510,820 US20070134247A9 (en) | 2002-04-12 | 2003-04-14 | Prevention of brain inflammation as a result of induced autoimmune response |
US12/467,931 US20090280114A1 (en) | 2002-04-12 | 2009-05-18 | Prevention of brain inflammation as a result of induced autoimmune response |
Applications Claiming Priority (2)
Application Number | Priority Date | Filing Date | Title |
---|---|---|---|
US37171902P | 2002-04-12 | 2002-04-12 | |
US60/371,719 | 2002-04-12 |
Related Child Applications (1)
Application Number | Title | Priority Date | Filing Date |
---|---|---|---|
US12/467,931 Continuation-In-Part US20090280114A1 (en) | 2002-04-12 | 2009-05-18 | Prevention of brain inflammation as a result of induced autoimmune response |
Publications (2)
Publication Number | Publication Date |
---|---|
WO2003086310A2 true WO2003086310A2 (en) | 2003-10-23 |
WO2003086310A3 WO2003086310A3 (en) | 2004-02-19 |
Family
ID=29250730
Family Applications (1)
Application Number | Title | Priority Date | Filing Date |
---|---|---|---|
PCT/US2003/011316 WO2003086310A2 (en) | 2002-04-12 | 2003-04-14 | Prevention of brain inflammation as a result of induced autoimmune response |
Country Status (3)
Country | Link |
---|---|
US (1) | US20070134247A9 (en) |
AU (1) | AU2003226356A1 (en) |
WO (1) | WO2003086310A2 (en) |
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WO2006113347A2 (en) * | 2005-04-13 | 2006-10-26 | The University Of Tennessee Research Foundation | Diagnostic and therapeutic potential of immune globulin intravenous (igiv) products |
WO2006118959A2 (en) * | 2005-04-29 | 2006-11-09 | Rinat Neuroscience Corp. | Antibodies directed against amyloid-beta peptide and methods using same |
WO2007027714A2 (en) | 2005-08-31 | 2007-03-08 | Schering Corporation | Engineered anti-il-23 antibodies |
EP1766396A2 (en) * | 2004-06-07 | 2007-03-28 | Ramot at Tel-Aviv University Ltd. | Method of passive immunization against disease or disorder characterized by amyloid aggregation with diminished risk of neuroinflammation |
WO2008030251A1 (en) * | 2006-09-08 | 2008-03-13 | Georgetown University | Deglycosylated anti-amyloid beta antibodies |
WO2008076321A1 (en) | 2006-12-14 | 2008-06-26 | Schering Corporation | Engineered anti-tslp antibody |
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- 2003-04-14 AU AU2003226356A patent/AU2003226356A1/en not_active Abandoned
- 2003-04-14 WO PCT/US2003/011316 patent/WO2003086310A2/en not_active Application Discontinuation
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WO2000072880A2 (en) * | 1999-05-28 | 2000-12-07 | Neuralab Limited | Prevention and treatment of amyloidogenic disease |
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