<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Guo Y</submitter><funding>NCCIH NIH HHS</funding><funding>Medical Research Council</funding><funding>NCI NIH HHS</funding><funding>Wellcome Trust</funding><pagination>3336-44</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4648262</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>192(7)</volume><pubmed_abstract>Vitamin A deficiency leads to increased susceptibility to a spectrum of infectious diseases. The studies presented dissect the intrinsic role of each of the retinoic acid receptor (RAR) isoforms in the clonal expansion, differentiation, and survival of pathogen-specific CD8 T cells in vivo. The data show that RAR? is required for the expression of gut-homing receptors on CD8(+) T cells and survival of CD8(+) T cells in vitro. Furthermore, RAR? is essential for survival of CD8(+) T cells in vivo following Listeria monocytogenes infection. In contrast, RAR? deletion leads to modest deficiency in Ag-specific CD8(+) T cell expansion during infection. The defective survival of RAR?-deficient CD8(+) T cells leads to a deficiency in control of L. monocytogenes expansion in the spleen. To our knowledge, these are the first comparative studies of the role of RAR isoforms in CD8(+) T cell immunity.</pubmed_abstract><journal>Journal of immunology (Baltimore, Md. : 1950)</journal><pubmed_title>Dissecting the role of retinoic acid receptor isoforms in the CD8 response to infection.</pubmed_title><pmcid>PMC4648262</pmcid><funding_grant_id>P30 CA023108</funding_grant_id><funding_grant_id>091823</funding_grant_id><funding_grant_id>R01AT005382</funding_grant_id><funding_grant_id>R01 AT005382</funding_grant_id><funding_grant_id>MR/J006742/1</funding_grant_id><pubmed_authors>Lee YC</pubmed_authors><pubmed_authors>Zhang W</pubmed_authors><pubmed_authors>Usherwood E</pubmed_authors><pubmed_authors>Guo Y</pubmed_authors><pubmed_authors>Noelle RJ</pubmed_authors><pubmed_authors>Brown C</pubmed_authors></additional><is_claimable>false</is_claimable><name>Dissecting the role of retinoic acid receptor isoforms in the CD8 response to infection.</name><description>Vitamin A deficiency leads to increased susceptibility to a spectrum of infectious diseases. The studies presented dissect the intrinsic role of each of the retinoic acid receptor (RAR) isoforms in the clonal expansion, differentiation, and survival of pathogen-specific CD8 T cells in vivo. The data show that RAR? is required for the expression of gut-homing receptors on CD8(+) T cells and survival of CD8(+) T cells in vitro. Furthermore, RAR? is essential for survival of CD8(+) T cells in vivo following Listeria monocytogenes infection. In contrast, RAR? deletion leads to modest deficiency in Ag-specific CD8(+) T cell expansion during infection. The defective survival of RAR?-deficient CD8(+) T cells leads to a deficiency in control of L. monocytogenes expansion in the spleen. To our knowledge, these are the first comparative studies of the role of RAR isoforms in CD8(+) T cell immunity.</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Apr</publication><modification>2020-10-29T10:43:21Z</modification><creation>2019-03-27T02:02:06Z</creation></dates><accession>S-EPMC4648262</accession><cross_references><pubmed>24610012</pubmed><doi>10.4049/jimmunol.1301949</doi></cross_references></HashMap>