Transcriptome analysis of Germinal Center and naïve B cells from miR-217TG and control mice by RNAseq
microRNAs (miRNAs) regulate virtually all biological processes, but little is known of their role in germinal center (GC) B cells. While the GC reaction is crucial to ensure a competent immune response, GC B cells are also the origin of most human lymphomas. Here we report that miR-217 is specifically upregulated in GC B cells. Gain- and loss-of-function mouse models reveal that miR-217 functions as a positive modulator of the GC response through the regulation of a DNA repair gene network. Moreover, we show that miR-217 overexpression promotes mature B cell lymphomagenesis. Therefore miR-217 provides a novel molecular link between the normal GC response and B cell transformation Overall design: 4 samples were analyzed by RNAseq: 1) naïve (CD19+Fas-GL7-) B cells from miR-217TG,  2) GC (CD19+Fas+GL7+) B cells from miR-217TG, 3) naïve (CD19+Fas-GL7-) B cells from  littermate controls and 4) GC (CD19+Fas+GL7+) B cells from littermate controls.  Samples were isolated by cell sorting from pooled Peyer’s patches (4-6 animals per genotype). Two independent experiments were performed.