US2018078539A1PendingUtilityA1

T-cell regulation in t-cell mediated diseases by reducing pathogenic function of th17 in a human subject through treatment with a nitroxide

Assignee: HABASH LOUISPriority: Mar 23, 2016Filed: Nov 27, 2017Published: Mar 22, 2018
Est. expiryMar 23, 2036(~9.7 yrs left)· nominal 20-yr term from priority
Inventors:Louis Habash
A61K 31/445
58
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Claims

Abstract

A method of reducing pathogenic T-helper cell activity in a human subject in need thereof is disclosed. The method comprises administering to the human subject, known to have a condition mediated by one or more differentiated T-helper cells responsive to Cd51, an effective amount of a nitroxide antioxidant, where the nitroxide antioxidant increases Cd51 expression, thereby reducing pathogenic T-helper cell activity. In some embodiments, the condition is an autoimmune disease.

Claims

exact text as granted — not AI-modified
What is claimed is: 
     
         1 . A method of reducing pathogenic T-helper cell activity in a human subject in need thereof, the method comprising:
 administering to the human subject, known to have a condition mediated by one or more differentiated T-helper cells responsive to Cd51, an effective amount of a nitroxide antioxidant, wherein the nitroxide antioxidant increases Cd51 expression, thereby reducing pathogenic T-helper cell activity.   
     
     
         2 . The method of  claim 1 , wherein the human subject is further known to have a disease associated with a decrease in Cd51 expression. 
     
     
         3 . The method of  claim 1 , wherein the nitroxide antioxidant is 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl. 
     
     
         4 . The method of  claim 1 , wherein the T-helper cell responsive to Cd51 is a Th17 cell. 
     
     
         5 . The method of  claim 4 , wherein the nitroxide antioxidant alters lipid biosynthesis within the Th17 cell. 
     
     
         6 . The method of  claim 5 , where the human subject is further known to have a disease mediated by IL-23 as an effector molecule. 
     
     
         7 . The method of  claim 1 , wherein the condition is associated with pathogenic activity of the one or more differentiated T-helper cells, wherein one or more effector molecules binds to the one or more differentiated T-helper cells. 
     
     
         8 . A method of inhibiting development of an autoimmune disease, comprising:
 administering to a human subject, known to be at risk of developing a disease mediated by pathogenic T-helper cell activity, an effective amount of a nitroxide antioxidant, wherein the pathogenic T-helper cell activity is inhibited, thereby inhibiting development of the autoimmune disease.   
     
     
         9 . The method of  claim 8 , wherein the human subject exhibits no outward symptoms of the autoimmune disease. 
     
     
         10 . The method of  claim 8 , further comprising identifying the human subject. 
     
     
         11 . The method of  claim 8 , wherein the nitroxide antioxidant increases Cd51 expression. 
     
     
         12 . The method of  claim 8 , wherein the nitroxide antioxidant is 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl. 
     
     
         13 . The method of  claim 8 , wherein the pathogenic T-helper cell is a Th17 cell, and wherein the nitroxide antioxidant alters lipid biosynthesis within the Th17 cell. 
     
     
         14 . The method of  claim 13 , wherein the autoimmune disease is further mediated by IL-23 as an effector molecule.

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