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Rheumatology Advance Access published online on February 23, 2008
Rheumatology, doi:10.1093/rheumatology/ken013
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Is Inhibitor of differentiation 3 involved in human primary Sjögren's syndrome?

J. Sellam1,*, C. Miceli-Richard1,*, J.-E. Gottenberg1, A. Proust2, M. Ittah1, F. Lavie1, P. Loiseau3 and X. Mariette1

1Rhumatologie and 2Hématologie, INSERM U802, Hôpital Bicêtre, Assistance Publique des Hôpitaux de Paris (AP-HP), Université Paris-Sud, Le Kremlin Bicêtre and 3Immunologie et Histocompatibilité, INSERM U396, Hôpital Saint-Louis, AP-HP, Paris, France.

Correspondence to: X. Mariette, Service de Rhumatologie, Hôpital de Bicêtre, 78 rue du Général Leclerc, 94275 Le Kremlin Bicêtre. E-mail: xavier.mariette{at}bct.aphp.fr


  Abstract

Objectives. 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.

Conclusion. 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.

KEY WORDS: Sjögren's syndrome, Inhibitor of differentiation 3, Mouse model, T cells, Genetic polymorphism, Anti-SSA/SSB, Salivary gland epithelial cell

*J. Sellam and C. Miceli-Richard equally contributed to this work.

Submitted 17 August 2007; revised version accepted 7 January 2008.
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