E-GEOD-45122 - MicroRNA-155 confers encephalogenic potential to Th17 cells by promoting IL-23 responsiveness and effector gene expression

Released on 1 May 2013, last updated on 2 June 2014
Mus musculus
Samples (4)
Array (1)
Protocols (7)
We examined the role of miR-155 in differentiated Th17 cells during their induction of Experimental Autoimmune Encephalomyelitis (EAE). Using adoptive transfer experiments, we found that highly purified, MOG antigen specific Th17 cells lacking miR-155 are defective in their capacity to cause EAE. Gene expression profiling of purified miR-155-/- IL-17F+ Th17 cells identified a subset of effector genes that are dependent upon miR-155 for their proper expression through a mechanism involving repression of the transcription factor Ets1. Among the genes reduced in the absence of miR-155 was IL-23R, resulting in miR-155-/- Th17 cells being hypo-responsive to IL-23. Taken together, our study demonstrates a critical role for miR-155 in Th17 cells as they unleash autoimmune inflammation, and finds that this occurs through a signaling network involving miR-155, Ets1 and the clinically relevant IL-23-IL-23R pathway. two biological replicates of miR-155-/- CD4+ IL-17F RFP+ T cells compared to two biological replicates of miR-155+/+CD4+IL-17F RFP+ T cells (as a control).
Experiment type
transcription profiling by array 
Brett Milash <brett.milash@hci.utah.edu>, Dominique A Kagele, Erin Bake, June L Round, Marah C Runtsch, Ruozhen Hu, Ryan M O'Connell, Thomas B Huffaker
Investigation descriptionE-GEOD-45122.idf.txt
Sample and data relationshipE-GEOD-45122.sdrf.txt
Raw data (1)E-GEOD-45122.raw.1.zip
Processed data (1)E-GEOD-45122.processed.1.zip
Array designA-GEOD-10787.adf.txt