Histone deacetylase (HDAC) inhibitors stimulate T-reg Cells
Posted: Tue Oct 16, 2007 2:26 am
Cancer drugs could fight autoimmune disease
* 16 October 2007
* NewScientist.com news service
Many anti-cancer drugs have the unfortunate side-effect of depressing the body's immune system. So it makes sense that one class of these drugs is being investigated as a way of tackling autoimmune diseases like multiple sclerosis and rheumatoid arthritis. These are triggered when the immune system's T-cells go into overdrive and attack the body's own cells.
Wayne Hancock and colleagues at the Children's Hospital of Philadelphia have now discovered that histone deacetylase (HDAC) inhibitors - drugs approved for treating cancers like lymphomas - stimulate a specific class of immune cells called regulatory T-cells. These control the activity of other immune cells, including rogue T-cells. In tests on mice, HDAC inhibitors suppressed inflammatory bowel disease and prevented rejection of heart and pancreatic grafts (Nature Medicine, DOI: 10.1038/nm1652).
Hancock believes the drugs do this by boosting both the number of regulatory T-cells and the amount of Foxp3, a messaging molecule they produce. This surfeit of Foxp3 in turn suppresses the immune response of T-cells.
* 16 October 2007
* NewScientist.com news service
Many anti-cancer drugs have the unfortunate side-effect of depressing the body's immune system. So it makes sense that one class of these drugs is being investigated as a way of tackling autoimmune diseases like multiple sclerosis and rheumatoid arthritis. These are triggered when the immune system's T-cells go into overdrive and attack the body's own cells.
Wayne Hancock and colleagues at the Children's Hospital of Philadelphia have now discovered that histone deacetylase (HDAC) inhibitors - drugs approved for treating cancers like lymphomas - stimulate a specific class of immune cells called regulatory T-cells. These control the activity of other immune cells, including rogue T-cells. In tests on mice, HDAC inhibitors suppressed inflammatory bowel disease and prevented rejection of heart and pancreatic grafts (Nature Medicine, DOI: 10.1038/nm1652).
Hancock believes the drugs do this by boosting both the number of regulatory T-cells and the amount of Foxp3, a messaging molecule they produce. This surfeit of Foxp3 in turn suppresses the immune response of T-cells.