<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE167943" accession="SRP308680">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP308680</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA705648</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE167943</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Reduced TCR?d signal strength engages phosphatidylinositol 3-kinase (PI3K) to drive thymic development of IL-17A-secreting  ?d T cells</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>Reduced TCR?d signal strength manifest by constrained Syk activity engages PI3K to maintain expression of key master regulators of the IL-17 program; ROR?t and c-Maf, and drive thymic development of IL-17A-secreting ?d T cells (?d17 cells). Notably, inhibition of PI3K not only abrogates ?d17 cell development, but also permits ?d progenitors to adopt a type-I interferon gene expression signature that identifies a novel CD8(+)Sca-1(+) ?d T cell subset. Overall design: Total ?d T cells were sorted from foetal C57BL/6 thymic lobes cultured for 8 days in the presence of a pan-PI3K inhibitor (ZSTK474) or under control conditions.</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE167943</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>34285131</ID>
        </XREF_LINK>
      </STUDY_LINK>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>38802512</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
  </STUDY>
</STUDY_SET>
