Inhibiting an enzyme prevented mice from developing a multiple sclerosis-like disease, a European study reports.
The finding about HDAC1, a member of the histone deacetylases family of enzymes, could open up new therapy possibilities for MS.
Researchers published their study, “A T cell-specific deletion of HDAC1 protects against experimental autoimmune encephalomyelitis,” in the Journal of Autoimmunity.
HDAC enzymes are responsible for which genes are turned on and which are turned off. A gene that is turned on will generate proteins, while one turned off will not.
Eighteen HDACs take part in the epigenetic process of turning genes on or off. In addition to regulating gene activity, they can change the activity and function of proteins. The bottom line is that they play a major role in regulating a cell’s behavior.
Previous studies have demonstrated that HDACs are particularly important to the regulation of immune T-cells’ response and communication. The research has also shown that inhibiting the enzymes diminishes immune response in mouse models, including mice with autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis.
The role that different HDAC family members play in the development of autoimmune disorders such as multiple sclerosis has been unclear, however.
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