<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Swain S</submitter><funding>Crohn&amp;apos;s and Colitis Foundation of America</funding><funding>NIDDK NIH HHS</funding><funding>Ruth K. Broad Biomedical Research Foundation</funding><funding>Crohn's &amp; Colitis Foundation</funding><funding>National Institutes of Health</funding><funding>M.J. Murdock Charitable Trust</funding><funding>NIGMS NIH HHS</funding><pagination>2989</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6308147</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>9</volume><pubmed_abstract>Dendritic cell (DC) expression of CD103, the α subunit of αEβ7 integrin, is thought to enable DC interactions with E-cadherin-expressing gastrointestinal epithelia for improved mucosal immunosurveillance. In the stomach, efficient DC surveillance of the epithelial barrier is crucial for the induction of immune responses to &lt;i>H. pylori&lt;/i>, the causative agent of peptic ulcers and gastric cancer. However, gastric DCs express only low levels of surface CD103, as we previously showed. We here tested the hypothesis that intracellular pools of CD103 in human gastric DCs can be redistributed to the cell surface for engagement of epithelial cell-expressed E-cadherin to promote DC-epithelial cell adhesion. In support of our hypothesis, immunofluorescence analysis of tissue sections showed that CD</pubmed_abstract><journal>Frontiers in immunology</journal><pubmed_title>CD103 (αE Integrin) Undergoes Endosomal Trafficking in Human Dendritic Cells, but Does Not Mediate Epithelial Adhesion.</pubmed_title><pmcid>PMC6308147</pmcid><funding_grant_id>GM110732</funding_grant_id><funding_grant_id>R03 DK107960</funding_grant_id><funding_grant_id>K01 DK097144</funding_grant_id><funding_grant_id>294174</funding_grant_id><funding_grant_id>P30 GM110732</funding_grant_id><pubmed_authors>Sidar B</pubmed_authors><pubmed_authors>Dankoff J</pubmed_authors><pubmed_authors>VanAusdol R</pubmed_authors><pubmed_authors>Smythies LE</pubmed_authors><pubmed_authors>Smith PD</pubmed_authors><pubmed_authors>Swain S</pubmed_authors><pubmed_authors>Sebrell TA</pubmed_authors><pubmed_authors>Roe MM</pubmed_authors><pubmed_authors>Bimczok D</pubmed_authors></additional><is_claimable>false</is_claimable><name>CD103 (αE Integrin) Undergoes Endosomal Trafficking in Human Dendritic Cells, but Does Not Mediate Epithelial Adhesion.</name><description>Dendritic cell (DC) expression of CD103, the α subunit of αEβ7 integrin, is thought to enable DC interactions with E-cadherin-expressing gastrointestinal epithelia for improved mucosal immunosurveillance. In the stomach, efficient DC surveillance of the epithelial barrier is crucial for the induction of immune responses to &lt;i>H. pylori&lt;/i>, the causative agent of peptic ulcers and gastric cancer. However, gastric DCs express only low levels of surface CD103, as we previously showed. We here tested the hypothesis that intracellular pools of CD103 in human gastric DCs can be redistributed to the cell surface for engagement of epithelial cell-expressed E-cadherin to promote DC-epithelial cell adhesion. In support of our hypothesis, immunofluorescence analysis of tissue sections showed that CD</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018</publication><modification>2026-06-19T03:14:39.26Z</modification><creation>2026-06-19T03:07:40.571Z</creation></dates><accession>S-EPMC6308147</accession><cross_references><pubmed>30622531</pubmed><doi>10.3389/fimmu.2018.02989</doi></cross_references></HashMap>