title: Is Inhibitor of differentiation 3 involved in human primary Sjögren's syndrome?
abstract: OBJECTIVE
  Inhibitor of differentiation 3 (Id3)-deficient mice show sicca symptoms, lymphocyte infiltration of exocrine glands and positive anti-Ro/SSA and anti-La/SSB antibodies, all hallmarks of primary Sjögren's syndrome (pSS). The impairment of Id3 in T cells and, possibly, in salivary glandular epithelial cells (SGECs) seems to be involved. This animal model prompted us to investigate the role of Id3 in human pSS.
  
  
  METHODS
  Quantitative Id3 expression in peripheral T cells, cultured SGECs and in total minor salivary glands was assessed by RT-PCR in pSS patients and controls. After Id3 sequencing, we investigated two single nucleotide polymorphisms (SNPs) (c.313G>A and g.-156A>G) in a case-control study of 212 Caucasian pSS patients and 168 controls.
  
  
  RESULTS
  Quantitative Id3 expression was not decreased in pSS patients nor in SGECs, in T cells or in minor salivary glands. As well, patients and controls did not differ in allele and genotype frequencies of Id3 SNPs (P = 0.67 and P = 0.71 for the c.313G>A and the g.-156A>G, respectively). Neither SNP was associated with a pattern of autoantibody secretion.
  
  
  CONCLUSIONS
  Although the Id3-deficient mouse model represents an attractive model for human pSS, Id3 expression is not impaired in SGECs, peripheral T cells and in labial salivary glands in pSS patients and Id3-relevant SNPs do not give evidence of genetic predisposition in Caucasian pSS patients.
authors.affiliation: Rhumatologie, INSERM U802, Hôpital Bicêtre, Assistance Publique des Hôpitaux de Paris, Université Paris-Sud, Le Kremlin Bicêtre, France.
authors.forename: J
authors.initials: J
authors.lastname: Sellam
authors.forename: C
authors.initials: C
authors.lastname: Miceli-Richard
authors.forename: J-E
authors.initials: JE
authors.lastname: Gottenberg
authors.forename: A
authors.initials: A
authors.lastname: Proust
authors.forename: M
authors.initials: M
authors.lastname: Ittah
authors.forename: F
authors.initials: F
authors.lastname: Lavie
authors.forename: P
authors.initials: P
authors.lastname: Loiseau
authors.forename: X
authors.initials: X
authors.lastname: Mariette
mesh_terms: D001323:Autoantibodies / Q000378:metabolism; D016022:Case-Control Studies; D002478:Cells, Cultured; D005260:Female; D015870:Gene Expression; D005787:Gene Frequency; D006801:Humans; D051796:Inhibitor of Differentiation Proteins / Q000096:biosynthesis* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000096:biosynthesis* / Q000235:genetics; D020641:Polymorphism, Single Nucleotide; D012333:RNA, Messenger / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D012470:Salivary Glands, Minor / Q000378:metabolism; D012859:Sjogren's Syndrome / Q000235:genetics / Q000276:immunology / Q000378:metabolism*
chemical_list: D001323:Autoantibodies; D051796:Inhibitor of Differentiation Proteins; D009363:Neoplasm Proteins; D012333:RNA, Messenger; C075640:ID3 protein, human