Histone/protein deacetylase 11 targeting promotes Foxp3+ Treg function

A visiting scholar from Shanghai, Dr. Jianbing Huang, along with our own mighty Liqing Wang, studied the effects of genetic and pharmacologic targeting of Hdac11 in mice. Deletion of Hdac11 in Foxp3+ Tregs, or its pharmacologic inhibition, enhanced Treg function and promoted cardiac allograft survival. This work highlights the potential importance of a little studied Hdac in the development of new therapies for use in transplantation and various autoimmune diseases.

Histone/protein deacetylase 11 targeting promotes Foxp3+ Treg function. Huang J, Wang L, Dahiya S, Han R, Samanta A, Beier UH, Bhatti TR, Bergman J, Sotomayor EM, Seto E, Kozikowski AP, Hancock WW. Scientific Reports.