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Is Inhibitor of differentiation 3 involved in human primary Sjögren's syndrome?
Rheumatology (Oxford). 2008 Apr; 47(4):437-41.R

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.

Authors+Show Affiliations

Rhumatologie, INSERM U802, Hôpital Bicêtre, Assistance Publique des Hôpitaux de Paris, Université Paris-Sud, Le Kremlin Bicêtre, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18296721

Citation

Sellam, J, et al. "Is Inhibitor of Differentiation 3 Involved in Human Primary Sjögren's Syndrome?" Rheumatology (Oxford, England), vol. 47, no. 4, 2008, pp. 437-41.
Sellam J, Miceli-Richard C, Gottenberg JE, et al. Is Inhibitor of differentiation 3 involved in human primary Sjögren's syndrome? Rheumatology (Oxford). 2008;47(4):437-41.
Sellam, J., Miceli-Richard, C., Gottenberg, J. E., Proust, A., Ittah, M., Lavie, F., Loiseau, P., & Mariette, X. (2008). Is Inhibitor of differentiation 3 involved in human primary Sjögren's syndrome? Rheumatology (Oxford, England), 47(4), 437-41. https://doi.org/10.1093/rheumatology/ken013
Sellam J, et al. Is Inhibitor of Differentiation 3 Involved in Human Primary Sjögren's Syndrome. Rheumatology (Oxford). 2008;47(4):437-41. PubMed PMID: 18296721.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Is Inhibitor of differentiation 3 involved in human primary Sjögren's syndrome? AU - Sellam,J, AU - Miceli-Richard,C, AU - Gottenberg,J-E, AU - Proust,A, AU - Ittah,M, AU - Lavie,F, AU - Loiseau,P, AU - Mariette,X, Y1 - 2008/02/23/ PY - 2008/2/26/pubmed PY - 2008/5/9/medline PY - 2008/2/26/entrez SP - 437 EP - 41 JF - Rheumatology (Oxford, England) JO - Rheumatology (Oxford) VL - 47 IS - 4 N2 - 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. SN - 1462-0332 UR - https://www.unboundmedicine.com/medline/citation/18296721/Is_Inhibitor_of_differentiation_3_involved_in_human_primary_Sjögren's_syndrome L2 - https://academic.oup.com/rheumatology/article-lookup/doi/10.1093/rheumatology/ken013 DB - PRIME DP - Unbound Medicine ER -