Specification of the T helper 17 (Th17) cell lineage requires a well-defined set 
of transcription factors, but how these integrate with posttranscriptional and 
epigenetic programs to regulate gene expression is poorly understood. Here we 
found defective Th17 cell cytokine expression in miR-155-deficient CD4+ T cells 
in vitro and in vivo. Mir155 was bound by Th17 cell transcription factors and 
was highly expressed during Th17 cell differentiation. miR-155-deficient Th17 
and T regulatory (Treg) cells expressed increased amounts of Jarid2, a 
DNA-binding protein that recruits the Polycomb Repressive Complex 2 (PRC2) to 
chromatin. PRC2 binding to chromatin and H3K27 histone methylation was increased 
in miR-155-deficient cells, coinciding with failure to express Il22, Il10, Il9, 
and Atf3. Defects in Th17 cell cytokine expression and Treg cell homeostasis in 
the absence of Mir155 could be partially suppressed by Jarid2 deletion. Thus, 
miR-155 contributes to Th17 cell function by suppressing the inhibitory effects 
of Jarid2.