Study holds hope for autoimmune diseases
PHILADELPHIA, March 7 (UPI) -- U.S. scientists have found a way to make regulatory immune cells function more efficiently, holding promise for such diseases as diabetes and arthritis.
One cause of an immune regulatory cell malfunction occurs when a mutation in the FOXP3 gene disables the immune cells' ability to function.
University of Pennsylvania researchers have found a way to modify enzymes that act on FOXP3, in turn making the regulatory immune cells work better.
Research associate Bin Li, first author of the study, determined when a set of enzymes called the histone acetyl transferases are turned on, or when another set called the histone deacetylases are turned off, the immune regulatory cells work better and longer. As a consequence, the FOXP3 protein functions to turn off pathways that would lead to autoimmune diseases.
"I think this simple approach will revolutionize the treatment of autoimmune diseases in humans because we have a new set of enzymatic drug targets as opposed to the non-specific therapies we now use," said senior author Dr. Mark Greene.
The research will appear online next week in the Proceedings of the National Academy of Sciences.
Copyright 2007 by United Press International.
PHILADELPHIA, March 7 (UPI) -- U.S. scientists have found a way to make regulatory immune cells function more efficiently, holding promise for such diseases as diabetes and arthritis.
One cause of an immune regulatory cell malfunction occurs when a mutation in the FOXP3 gene disables the immune cells' ability to function.
University of Pennsylvania researchers have found a way to modify enzymes that act on FOXP3, in turn making the regulatory immune cells work better.
Research associate Bin Li, first author of the study, determined when a set of enzymes called the histone acetyl transferases are turned on, or when another set called the histone deacetylases are turned off, the immune regulatory cells work better and longer. As a consequence, the FOXP3 protein functions to turn off pathways that would lead to autoimmune diseases.
"I think this simple approach will revolutionize the treatment of autoimmune diseases in humans because we have a new set of enzymatic drug targets as opposed to the non-specific therapies we now use," said senior author Dr. Mark Greene.
The research will appear online next week in the Proceedings of the National Academy of Sciences.
Copyright 2007 by United Press International.
Posts
