HDAC6 regulates IL-17 expression in T lymphocytes: implications for HDAC6-targeted therapies.

ABSTRACT: The pro-inflammatory cytokine interleukin 17 (IL-17) is critically involved in immunity and inflammation. T-helper 17 and γδ T cells are the predominant sources of IL-17 in the immune system. However, the mechanisms by which the expression of IL-17 is regulated in T cells remain elusive. Here, we demonstrate that loss of histone deacetylase 6 (HDAC6) in mice does not affect the generation of CD4⁺ or CD8⁺ T cells, but stimulates the development of IL-17-producing γδ T cells. Our data further show that HDAC6 deficiency increases the production of IL-17 by Vγ4⁺ γδ T cells in the spleen and lymph nodes. Consistent with these observations, small-molecule inhibition of HDAC6 activity in γδ T cells promotes the expression of IL-17 in vitro. These data thus

SUBMITTER: Yan B 

PROVIDER: S-EPMC5381261 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature