New pathway to combat autoimmune diseases

20 March 2007 Print this article Comments Share this article
New understanding of the FOXP3 protein pathway provides opportunities to improve the functioning of immune regulatory cells, with important implications for treating autoimmune-related diseases.Lead author Dr Bin Li (Department of Pathology and Laboratory Medicine, University of Pennsylvania) and colleagues write, "the forkhead family protein FOXP3 acts as a repressor of transcription and is both an essential and sufficient regulator of the development and function of regulatory T cells". However, the researchers point out that the mechanism by which FOXP3-mediated transcriptional repression occurs remains unclear.Through their research the group describes a mechanism which could be targeted by drugs to stabilise immune regulatory cells and combat autoimmune diseases, including multiple sclerosis, diabetes and arthritis.Li's team describes how the FOXP3 protein works via a complex set of enzymes including histone deacetylases (HD) and histone acetyl transferases (HAT). Should the HAT be turned on, or the HD turned off, the immune regulatory cells were reported to work better and for longer."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," adds co-author Mark Green."Before this work, FOXP3 was thought essential for regulatory T-cell function, but how FOXP3 worked was not known," says Li. "Our research identifies a critical mechanism. Based on this mechanism, treatments could be developed to modulate this regulatory cell population." "In this line of investigation, we have learned how to turn on or off this regulatory immune cell population - which is normally needed to prevent autoimmune diseases - using drugs that are approved for other purposes, but work on these enzymes" notes co-author Sandra Saouaf.Reference...

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