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Loss of HDAC11 leads to reduced secretion of MCP-1 and less severe EAE

ABSTRACT: HDAC11 regulates IL-10 expression and overexpression of HDAC11 in antigen presenting cells (APCs) leads to a pro-inflammatory phenotype. Conversely, loss of HDAC11 leads to upregulation of IL-10 and immune tolerance. HDAC11 overexpression is also associated with inflammatory diseases including multiple sclerosis. Hence we wished to determine the inflammatory mediators regulated by HDAC11. We used microarray to determine gene expression profile of macrophages from WT and HDAC11 knockout mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE56366 | GEO | 2014/03/31

SECONDARY ACCESSION(S): PRJNA243058

REPOSITORIES: GEO

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Loss of HDAC11 leads to reduced secretion of MCP-1 and less severe EAE

Project description:HDAC11 regulates IL-10 expression and overexpression of HDAC11 in antigen presenting cells (APCs) leads to a pro-inflammatory phenotype. Conversely, loss of HDAC11 leads to upregulation of IL-10 and immune tolerance. HDAC11 overexpression is also associated with inflammatory diseases including multiple sclerosis. Hence we wished to determine the inflammatory mediators regulated by HDAC11. We used microarray to determine gene expression profile of macrophages from WT and HDAC11 knockout mice. Thioglycollate induced-peritoneal macrophages obtained from WT and HDAC11 knockout mice were used for total RNA extraction to determine changes in gene expression levels in macrophages from WT and HDAC11 knockout mice.

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