{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gleason MK"],"funding":["NIAID NIH HHS","NHLBI NIH HHS","NCI NIH HHS"],"pagination":["3064-72"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3321868"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["119(13)"],"pubmed_abstract":["NK-cell function is regulated by the integration of signals received from activating and inhibitory receptors. Here we show that a novel immune receptor, T-cell Ig and mucin-containing domain-3 (Tim-3), is expressed on resting human NK cells and is up-regulated on activation. The NK92 NK-cell line engineered to overexpress Tim-3 showed a marked increase in IFN-γ production in the presence of soluble rhGal-9 or Raji tumor cells engineered to express Gal-9. The Tim-3(+) population of low-dose IL-12/IL-18-activated primary NK cells significantly increased IFN-γ production in response to soluble rhGal-9, Gal-9 presented by cell lines, and primary acute myelogenous leukemia (AML) targets that endogenously express Gal-9. This effect is highly specific as Tim-3 Ab blockade significantly decreased"],"journal":["Blood"],"pubmed_title":["Tim-3 is an inducible human natural killer cell receptor that enhances interferon gamma production in response to galectin-9."],"pmcid":["PMC3321868"],"funding_grant_id":["R01 HL55417","R01 CA72669","P01 CA065493","R01 HL055417","P30-CA77598","P30 CA077598","P01 AI056299","R01 CA072669","P01 CA111412","R01 HL056067","P01-CA111412-01"],"pubmed_authors":["Cooley SA","Miller JS","Verneris MR","Panoskaltsis-Mortari A","O'Brien MS","Blazar BR","McCullar V","Gleason MK","Lenvik TR","Cichocki F","Hirashima M","Holman CJ","Niki T","Felices M"],"additional_accession":[]},"is_claimable":false,"name":"Tim-3 is an inducible human natural killer cell receptor that enhances interferon gamma production in response to galectin-9.","description":"NK-cell function is regulated by the integration of signals received from activating and inhibitory receptors. Here we show that a novel immune receptor, T-cell Ig and mucin-containing domain-3 (Tim-3), is expressed on resting human NK cells and is up-regulated on activation. The NK92 NK-cell line engineered to overexpress Tim-3 showed a marked increase in IFN-γ production in the presence of soluble rhGal-9 or Raji tumor cells engineered to express Gal-9. The Tim-3(+) population of low-dose IL-12/IL-18-activated primary NK cells significantly increased IFN-γ production in response to soluble rhGal-9, Gal-9 presented by cell lines, and primary acute myelogenous leukemia (AML) targets that endogenously express Gal-9. This effect is highly specific as Tim-3 Ab blockade significantly decreased","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 Mar","modification":"2025-04-04T21:05:11.466Z","creation":"2019-03-27T00:52:04Z"},"accession":"S-EPMC3321868","cross_references":{"pubmed":["22323453"],"doi":["10.1182/blood-2011-06-360321"]}}