{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Guo Y"],"funding":["NCCIH NIH HHS","Medical Research Council","NCI NIH HHS","Wellcome Trust"],"pagination":["3336-44"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4648262"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["192(7)"],"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."],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["Dissecting the role of retinoic acid receptor isoforms in the CD8 response to infection."],"pmcid":["PMC4648262"],"funding_grant_id":["P30 CA023108","091823","R01AT005382","R01 AT005382","MR/J006742/1"],"pubmed_authors":["Lee YC","Zhang W","Usherwood E","Guo Y","Noelle RJ","Brown C"],"additional_accession":[]},"is_claimable":false,"name":"Dissecting the role of retinoic acid receptor isoforms in the CD8 response to infection.","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.","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Apr","modification":"2020-10-29T10:43:21Z","creation":"2019-03-27T02:02:06Z"},"accession":"S-EPMC4648262","cross_references":{"pubmed":["24610012"],"doi":["10.4049/jimmunol.1301949"]}}