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n‐Butyrate Anergized Effector CD4 + T Cells Independent of Regulatory T cell Generation or Activity
Author(s) -
Fontenelle B.,
Gilbert K. M.
Publication year - 2012
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2012.02740.x
Subject(s) - butyrate , foxp3 , t cell , microbiology and biotechnology , cytotoxic t cell , histone deacetylase , biology , secretion , interleukin 21 , chemistry , immunology , in vitro , immune system , histone , biochemistry , fermentation , gene
CD4 + T cell anergy reflects the inability of CD4 + T cells to respond functionally to antigenic stimulation through proliferation or IL‐2 secretion. Histone deacetylase (HDAC) inhibitors have been shown to induce anergy in antigen‐activated CD4 + T cells. However, questions remain if HDAC inhibitors mediate anergy through direct action upon activated CD4 + T cells or through the generation and/or enhancement of regulatory T (T reg ) cells. To assess if HDAC inhibitor n‐butyrate induces anergy independent of the generation or expansion of FoxP3 + T reg cells in vitro , we examine n‐butyrate‐treated murine CD4 + T cells for anergy induction and FoxP3 + T reg activity. Whereas n‐butyrate decreases CD4 + T cell proliferation and IL‐2 secretion, n‐butyrate did not augment FoxP3 protein production or confer a suppressive phenotype upon CD4 + T cells. Collectively, these data suggest that HDAC inhibitors can facilitate CD4 + T cell functional unresponsiveness directly and independently of T reg cell involvement.