<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Luther SA</submitter><funding>NIAID NIH HHS</funding><pagination>12694-9</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC18826</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>97(23)</volume><pubmed_abstract>The spontaneous mutant mouse strain, plt/plt, lacks the secondary lymphoid organ chemokine (SLC)-ser gene and has disrupted trafficking of T cells and dendritic cells (DCs) to lymphoid tissues. We demonstrate here that the gene for the related chemokine, Epstein-Barr virus-induced molecule-1 ligand chemokine (ELC), is also deleted in this immunodeficient mouse strain. Using a combination of approaches, including bone marrow reconstitution and double in situ hybridization, we show in wild-type mice that ELC is expressed by T zone stromal cells that also make SLC. Smaller amounts of ELC are made by DCs, predominantly of the CD8(+) phenotype. We propose that ELC- and SLC-expressing T zone stromal cells play a central role in bringing naive T cells and DCs together for the initiation of immune</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>Coexpression of the chemokines ELC and SLC by T zone stromal cells and deletion of the ELC gene in the plt/plt mouse.</pubmed_title><pmcid>PMC18826</pmcid><funding_grant_id>R01 AI045073</funding_grant_id><funding_grant_id>AI45073</funding_grant_id><pubmed_authors>Tang HL</pubmed_authors><pubmed_authors>Cyster JG</pubmed_authors><pubmed_authors>Hyman PL</pubmed_authors><pubmed_authors>Luther SA</pubmed_authors><pubmed_authors>Farr AG</pubmed_authors></additional><is_claimable>false</is_claimable><name>Coexpression of the chemokines ELC and SLC by T zone stromal cells and deletion of the ELC gene in the plt/plt mouse.</name><description>The spontaneous mutant mouse strain, plt/plt, lacks the secondary lymphoid organ chemokine (SLC)-ser gene and has disrupted trafficking of T cells and dendritic cells (DCs) to lymphoid tissues. We demonstrate here that the gene for the related chemokine, Epstein-Barr virus-induced molecule-1 ligand chemokine (ELC), is also deleted in this immunodeficient mouse strain. Using a combination of approaches, including bone marrow reconstitution and double in situ hybridization, we show in wild-type mice that ELC is expressed by T zone stromal cells that also make SLC. Smaller amounts of ELC are made by DCs, predominantly of the CD8(+) phenotype. We propose that ELC- and SLC-expressing T zone stromal cells play a central role in bringing naive T cells and DCs together for the initiation of immune</description><dates><release>2000-01-01T00:00:00Z</release><publication>2000 Nov</publication><modification>2025-04-04T22:06:25.574Z</modification><creation>2019-03-26T23:45:22Z</creation></dates><accession>S-EPMC18826</accession><cross_references><pubmed>11070085</pubmed><doi>10.1073/pnas.97.23.12694</doi></cross_references></HashMap>