title: Polymorphisms in the selenoprotein S gene: lack of association with autoimmune inflammatory diseases.
abstract: BACKGROUND
  Selenoprotein S (SelS) protects the functional integrity of the endoplasmic reticulum against the deleterious effects of metabolic stress. SEPS1/SelS polymorphisms have been involved in the increased release of pro-inflammatory cytokines interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and IL-6 in macrophages. We aimed at investigating the role of the SEPS1 variants previously associated with higher plasma levels of these cytokines and of the SEPS1 haplotypes in the susceptibility to develop immune-mediated diseases characterized by an inflammatory component.
  
  
  RESULTS
  Six polymorphisms distributed through the SEPS1 gene (rs11327127, rs28665122, rs4965814, rs12917258, rs4965373 and rs2101171) were genotyped in more than two thousand patients suffering from type 1 diabetes, rheumatoid arthritis or inflammatory bowel diseases and 550 healthy controls included in the case-control study.
  
  
  CONCLUSIONS
  Lack of association of SEPS1 polymorphisms or haplotypes precludes a major role of this gene increasing predisposition to these inflammatory diseases.
authors.affiliation: Immunology Department, Hospital Universitario San Carlos, Madrid, Spain. alfmdoncel@terra.es
authors.forename: Alfonso
authors.initials: A
authors.lastname: Martínez
authors.forename: Jose Luis
authors.initials: JL
authors.lastname: Santiago
authors.forename: Jezabel
authors.initials: J
authors.lastname: Varadé
authors.forename: Ana
authors.initials: A
authors.lastname: Márquez
authors.forename: José Ramón
authors.initials: JR
authors.lastname: Lamas
authors.forename: Juan Luis
authors.initials: JL
authors.lastname: Mendoza
authors.forename: Hermenegildo
authors.initials: H
authors.lastname: de la Calle
authors.forename: Manuel
authors.initials: M
authors.lastname: Díaz-Rubio
authors.forename: Emilio G
authors.initials: EG
authors.lastname: de la Concha
authors.forename: Benjamín
authors.initials: B
authors.lastname: Fernández-Gutiérrez
authors.forename: Elena
authors.initials: E
authors.lastname: Urcelay
mesh_terms: D000293:Adolescent; D000328:Adult; D001172:Arthritis, Rheumatoid / Q000235:genetics*; D016022:Case-Control Studies; D003093:Colitis, Ulcerative / Q000235:genetics*; D003424:Crohn Disease / Q000235:genetics*; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006239:Haplotypes; D006801:Humans; D008297:Male; D008565:Membrane Proteins / Q000235:genetics*; D008875:Middle Aged; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic; D051140:Selenoproteins / Q000235:genetics*; D013030:Spain
chemical_list: D008565:Membrane Proteins; C487710:SELENOS protein, human; D051140:Selenoproteins