{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jensen MA"],"funding":["NIDDK NIH HHS","NCRR NIH HHS","NIAID NIH HHS","NIAMS NIH HHS"],"pagination":["596-601"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3910490"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["72(4)"],"pubmed_abstract":["Objective
Hyperactivity of the type I interferon (IFN) pathway is involved in the pathogenesis of systemic lupus erythematosus (SLE). Immunoglobulin like transcript (ILT3) is an immunohibitory transmembrane molecule which is induced by type I IFNs. ILT3 is expressed by plasmacytoid dendritic cells (PDCs), monocytoid dendritic cells (MDCs), and monocytes/macrophages. Given the pathogenic role of IFN in SLE, we hypothesised that the IFN-induced immunosuppressive ILT3 receptor may be dysfunctional in human SLE.Methods
132 European-derived and 79 Hispanic-American SLE patients were genotyped for two coding-change single nucleotide polymorphisms (SNPs) predicted to interfere with protein folding in ILT3 (rs11540761 and rs1048801). 116 control DNA samples and sera from healthy co"],"journal":["Annals of the rheumatic diseases"],"pubmed_title":["Functional genetic polymorphisms in ILT3 are associated with decreased surface expression on dendritic cells and increased serum cytokines in lupus patients."],"pmcid":["PMC3910490"],"funding_grant_id":["UL1 RR024999","AI071651","P30 DK042086","K08 AI083790","P30 DK42086","L30 AI071651","R01 AR060861"],"pubmed_authors":["Jensen MA","Kumar AA","Kumabe M","Patterson KC","Franek BS","Niewold TB"],"additional_accession":[]},"is_claimable":false,"name":"Functional genetic polymorphisms in ILT3 are associated with decreased surface expression on dendritic cells and increased serum cytokines in lupus patients.","description":"Objective
Hyperactivity of the type I interferon (IFN) pathway is involved in the pathogenesis of systemic lupus erythematosus (SLE). Immunoglobulin like transcript (ILT3) is an immunohibitory transmembrane molecule which is induced by type I IFNs. ILT3 is expressed by plasmacytoid dendritic cells (PDCs), monocytoid dendritic cells (MDCs), and monocytes/macrophages. Given the pathogenic role of IFN in SLE, we hypothesised that the IFN-induced immunosuppressive ILT3 receptor may be dysfunctional in human SLE.Methods
132 European-derived and 79 Hispanic-American SLE patients were genotyped for two coding-change single nucleotide polymorphisms (SNPs) predicted to interfere with protein folding in ILT3 (rs11540761 and rs1048801). 116 control DNA samples and sera from healthy co","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 Apr","modification":"2026-05-03T02:14:12.262Z","creation":"2019-03-27T01:21:05Z"},"accession":"S-EPMC3910490","cross_references":{"pubmed":["22904259"],"doi":["10.1136/annrheumdis-2012-202024"]}}