<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE118166" accession="SRP156451">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP156451</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA484734</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE118166</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Dysbiotic microbiome triggers Th17 cells to mediate oral mucosal immunopathology in mice and humans</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>Animal model implicates microbiota-triggered oral mucosal Th17 cells as drivers of local immunopathology and therapeutic targets in periodontitis. Overall design: Total RNA from gingival tissues from mice undergoing experimental periodontitis . Each mouse has a ligated (induction site) side and a control side and mice are treated with an inhibitor of TH17 inflammation  (GSK805 (ROR?t Inverse Agonist II)) or vehicle control. We are interested in the differences in gingival inflammation in the presence/absence of the inhibitor. Mice have a strong response to treatment by clinical score.</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE118166</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>30333238</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
  </STUDY>
</STUDY_SET>
