Microglial Expression of Hdac1 and Hdac2 is Dispensable for Experimental Autoimmune Encephalomyelitis (EAE) Progression

Abstract

Previously, we reported that microglial expression of histone deacetylases 1 and 2 (Hdac1 and Hdac2) is required for microglial maturation and modulates disease progression in a mouse model of Alzheimer’s disease. Here, we analyze the role of microglial expression of Hdac1 and Hdac2 in another disease paradigm, namely experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. The aim of this study was to ascertain whether microglial expression of these two epigenetic regulators modulates disease progression in the context of autoimmune disease. Hdac1 and Hdac2 were knocked out either individually or in combination using a microglia-specific, tamoxifen-inducible Cre-deleter line (Cx3cr1-CreERT2). The clinical course as well as histopathological changes during EAE were assessed in adult mice lacking microglial expression of these genes. Overall, no differences in disease onset, progression or severity could be detected in mice lacking microglial expression of either one or both of Hdac1 and Hdac2 genes. Similarly, the histopathology showed no differences in lymphocyte or macrophage infiltration or demyelination in either of the analyzed groups. As such, we conclude that unlike in neurodegenerative disease, microglial expression of Hdac1 and Hdac2 does not play a role in EAE.

Keywords

• microglia
• experimental autoimmune encephalomyelitis
• Hdac1
• Hdac2
• epigenetics