<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE159418" accession="SRP287188">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP287188</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA668828</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE159418</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>IL-22-dependent dysbiosis and mononuclear phagocyte depletion contribute to steroid-resistant gut graft-versus-host disease in mice II</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Other"/>
      <STUDY_ABSTRACT>CD4+ and CD8+ T cells can reciprocally differentiate into Th/Tc1, Th/Tc17 and Th/Tc22. Although alloreactive Th/Tc1 cells play a critical role in initiating pathogenesis of gut acute graft-versus-host disease (Gut-aGVHD), the pathogenic T cells in steroid-resistant Gut-aGVHD (SR-Gut-aGVHD) remains unclear. Here, we show that in murine models of SR-Gut-aGVHD, the pathogenesis is associated with reduction of IFN-g+ Th/Tc1 and IL-17A+IL-22- Th/Tc17 cells but expansion of IL-17-IL-22+ Th/Tc22, particularly Tc22 cells. The IL-22 from Th/Tc22 cells causes dysbiosis. Overall design: Examination of gut microbiome difference in the mouse model of acute gut GVHD</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE159418</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>33547295</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
    <STUDY_ATTRIBUTES>
      <STUDY_ATTRIBUTE>
        <TAG>parent_bioproject</TAG>
        <VALUE>PRJNA668824</VALUE>
      </STUDY_ATTRIBUTE>
    </STUDY_ATTRIBUTES>
  </STUDY>
</STUDY_SET>
