US2006188499A1PendingUtilityA1

Methods of treating diseases which are mediated by cutaneous lymphocyte antigen positive cells

Individually held — no corporate assignee on recordPriority: Feb 14, 2005Filed: Feb 14, 2006Published: Aug 24, 2006
Est. expiryFeb 14, 2025(expired)· nominal 20-yr term from priority
A61P 37/04A61P 35/00A61P 31/22A61P 43/00A61P 37/08A61P 17/04C07K 16/244G01N 33/6881C07K 2317/76A61K 49/006A61P 17/02A61K 39/3955A61P 17/00G01N 33/505G01N 33/6869C07K 14/52A61P 17/14A61P 17/10A61K 49/0008C07K 16/2803A61K 2039/505A61K 2039/545
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Claims

Abstract

The present invention relates to methods of treating patients suffering from itching and puritis mediated by cutaneous lymphocyte antigen positive T cell. In particular, diseases or disorders including contact dermatitis, drug induced delayed type cutaneous allergic reactions, toxic epidermal necrolysis, cutaneous T cell lymphoma, bullous pemphigoid, alopecia aereata, vitiligo, acne rosacea, prurigo nodularis, and herpes simplex virus, or combination thereof will benefit from the administration of an IL-31 antagonist. The invention also includes methods of predicting a therapeutically responsive patient population.

Claims

exact text as granted — not AI-modified
1 . A method of treating diseased skin comprising administering an antagonist molecule to a mammal with the diseased skin wherein the diseased skin is characterized by cutaneous lymphocyte antigen positive T cells and the antagonist molecule specifically binds to the polypeptide comprising the amino acid sequence as shown in SEQ ID NO:2 or SEQ ID NO: 4, and whereby administration of the antagonist molecule improves, prevents, inhibits or reduces the diseased skin.  
     
     
         2 . The method according to  claim 1 , wherein the patient has a skin disorder selected from Contact dermatitis, Drug induced delayed type cutaneous allergic reactions, Toxic epidermal necrolysis, Cutaneous T cell Lymphoma, Bullous pemphigoid, Alopecia aereata, Vitiligo, Acne Rosacea, Prurigo nodularis, and Herpes simplex virus.  
     
     
         3 . The method according to  claim 2 , wherein the mammal is a human.  
     
     
         4 . The method according to  claim 1 , wherein the antagonist is an antibody or antibody fragment.  
     
     
         5 . The method according to  claim 4 , wherin the antagonist molecule specifically binds to the polypeptide comprising the amino acid sequence as shown in SEQ ID NO:2.  
     
     
         6 . The method according to  claim 1 , wherein the diseased skin is pruritic.  
     
     
         7 . A method for treating pruritis comprising administering an antagonist molecule to a mammal with the pruritis wherein the pruritis is characterized by cutaneous lymphocyte antigen positive T cells and wherein the antagonist molecule specifically binds to the polypeptide having the amino acid sequence as shown in SEQ ID NO:2 or in SEQ ID NO: 4, and whereby administration of the antagonist molecule improves, prevents, inhibits or reduces the pruritis.  
     
     
         8 . The method according to  claim 7 , wherein the pruritis is associated with a skin disorder selected from Contact dermatitis, Drug induced delayed type cutaneous allergic reactions, Toxic epidermal necrolysis, Cutaneous T cell Lymphoma, Bullous pemphigoid, Alopecia aereata, Vitiligo, Acne Rosacea, Prurigo nodularis, and Herpes simplex virus.  
     
     
         9 . The method according to  claim 8 , wherein the mammal is a human.  
     
     
         10 . The method according to  claim 7 , wherein the antagonist is an antibody or antibody fragment.  
     
     
         11 . The method according to  claim 10 , wherin the antagonist molecule specifically binds to the polypeptide comprising the amino acid sequence as shown in SEQ ID NO:2.  
     
     
         12 . A method for predicting therapeutic response to an IL-31 antagonist in an individual in need of IL-31 antagonist therapy comprising obtaining a biological sample from the patient, isolating circulating cutaneous lymphocyte positive T cells from the biological sample, and detecting IL-31 production from the isolated cutaneous lymphocyte positive T cells.  
     
     
         13 . The method according to  claim 12 , wherein the IL-31 is detected by specifically binding to an IL-31 antagonist.  
     
     
         14 . The method according to  claim 13 , wherein the IL-31 antagonist is an anti-IL-31 antibody or antibody fragment.  
     
     
         15 . The method according to  claim 12 , wherin the antagonist molecule specifically binds to the polypeptide comprising the amino acid sequence as shown in SEQ ID NO:2.  
     
     
         16 . The method according to  claim 12 , wherein the individual in need of IL-31 antagonist therapy has a skin disorder selected from Contact dermatitis, Drug induced delayed type cutaneous allergic reactions, Toxic epidermal necrolysis, Cutaneous T cell Lymphoma, Bullous pemphigoid, Alopecia aereata, Vitiligo, Acne Rosacea, Prurigo nodularis, and Herpes simplex virus.  
     
     
         17 . The method according to  claim 10 , comprising the additional step of stimulating or activating the cutaneous lymphocyte antigen positive T cells.  
     
     
         18 . The method according to  claim 17 , wherein the IL-31 is detected by specifically binding to an IL-31 antagonist.  
     
     
         19 . The method according to  claim 17 , wherein the IL-31 antagonist molecule is an anti-IL-31 antibody or antibody fragment.  
     
     
         20 . The method according to  claim 19 , wherin the antagonist molecule specifically binds to the polypeptide comprising the amino acid sequence as shown in SEQ ID NO:2.

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