%0 Journal Article
%T HDAC6 regulates IL-17 expression in T lymphocytes: implications for HDAC6-targeted therapies
%A Bing Yan
%A Dengwen Li
%A Hong Bai
%A Jun Zhou
%A Miao Chen
%A Min Liu
%A Songbo Xie
%A Yang Liu
%J Theranostics
%D 2017
%I Ivyspring International Publisher
%R 10.7150/thno.17615
%X The pro-inflammatory cytokine interleukin 17 (IL-17) is critically involved in immunity and inflammation. T-helper 17 and ¦Ã¦Ä 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 ¦Ã¦Ä T cells. Our data further show that HDAC6 deficiency increases the production of IL-17 by V¦Ã4+ ¦Ã¦Ä T cells in the spleen and lymph nodes. Consistent with these observations, small-molecule inhibition of HDAC6 activity in ¦Ã¦Ä T cells promotes the expression of IL-17 in vitro. These data thus reveal that HDAC6 represses IL-17 production in T cells, providing novel insights into the role of HDAC6 in the immune system. These findings also have important implications for the clinical investigation of HDAC6-targeted therapies.
%K histone deacetylase 6
%K interleukin 17
%K T cell
%K development
%K knockout mouse.
%U http://www.thno.org/v07p1002.htm