<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE64687" accession="SRP051727">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP051727</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA271681</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE64687</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Differences in murine miR-150-/- CD8+ T cells</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>MicroRNAs are a major class of gene regulators in mammals.  While numerous aspects of the immune systems are controlled by miRNAs, their precise role in the CD8+ T cell response remains unclear.  In this report, we show that miR-150 is the most abundant miRNA expressed in CD8+ T cells and its expression is required for proper effector cell differentiation in response to acute and chronic pathogens.  In the absence of miR-150, CD8+ T cells failed to both undergo robust expansion and differentiate into short-lived terminal effector cells. The lack of miR-150 also altered the effector CD8+ T cell transcriptome such that, despite activation, genes associated with naïve or memory cells were highly expressed.  The deletion of miR-150 also reduced killing efficiency of CD8+ T cells.  These results uncover a cell-intrinsic role for miR-150 in the regulation of CD8+ T cell effector fate and function. Overall design: mRNA and small RNAs were sequenced each from 2 biological replicates of wild-type and miR-150 KO CD8+ T cells</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE64687</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>26549197</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
  </STUDY>
</STUDY_SET>
