US2011243951A1PendingUtilityA1

Immunomodulating tumor necrosis factor receptor 25 (tnfr25) agonists, antagonists and immunotoxins

Assignee: UNIV MIAMIPriority: Aug 30, 2005Filed: Aug 3, 2009Published: Oct 6, 2011
Est. expiryAug 30, 2025(expired)· nominal 20-yr term from priority
A61P 43/00A61P 37/06A61P 37/02A61P 37/08A61P 37/04A61P 35/00A61P 31/00A61P 29/00A61K 2039/505C07K 16/2875C07K 2317/14C07K 16/241C07K 2317/76A61K 45/06A61K 38/1709C07K 2317/74A61P 11/00A61K 35/13C07K 16/2878A61P 11/06A61P 1/04A61K 39/3955C07K 2317/75A61K 40/4215A61K 40/22A61K 40/15A61K 40/11A61K 39/0011
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Claims

Abstract

It is an object of the invention to provide novel compositions and methods utilizing immunomodulating agents that can either stimulate or indirectly augment the immune system or in other cases have an immunosuppressive effect. TNFR25 agonists disclosed herein have an anti-inflammatory and healing effect. They can be used, among other things, to treat disease caused by asthma and chronic inflammation such as for example inflammatory bowel diseases including ulcerative colitis and Crohn's Disease. TNFR25 antagonists disclosed herein are capable of inhibiting CD8 T cell-mediated cellular immune responses and can for example, mitigate organ or tissue rejection following a tissue transplantation. TNFR25 agonists disclosed herein represent biological response modifiers that alter the interaction between the body's cellular immune defenses and cancer cells to boost, direct, or restore the body's ability to fight the cancer when given with tumor vaccines. TNFR25 specific immunotoxins disclosed herein are also capable of increasing the effectiveness of a chemotherapeutic regimen by depleting a cancer patient of naturally occurring immunosuppressive cells.

Claims

exact text as granted — not AI-modified
1 . (canceled) 
     
     
         2 . A method for inhibiting antigen-induced CD8 T cell expansion in a mammalian subject, the method comprising the step of administering to the subject a TNFR25 antagonist in an amount effective to inhibit antigen-induced CD8 T cell expansion in the subject. 
     
     
         3 . The method of  claim 2 , wherein the TNFR25 antagonist is an antibody. 
     
     
         4 . The method of  claim 3 , wherein the antibody is a monoclonal antibody that specifically binds TNFR25 but is not agonistic for TNFR25. 
     
     
         5 . The method of  claim 2 , wherein the antigen-induced CD8 T cell expansion contributes to inflammation of the subject's airway.

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