liu.seSearch for publications in DiVA
Change search
ReferencesLink to record
Permanent link

Direct link
Genetic associations to germinal centre formation in primary Sjogren's syndrome
University of Bergen, Norway / Uppsala University, Sweden .
Stavanger University Hospital, Norway.
University of Bergen, Norway .
Stavanger University Hospital, Norway.
Show others and affiliations
2014 (English)In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 73, no 6, 1253-1258 p.Article in journal (Refereed) Published
Abstract [en]

Background Primary Sjögren's syndrome (pSS) is an autoimmune rheumatic disease mainly characterised by focal mononuclear cell infiltration in the salivary and lacrimal glands, and by the symptoms xerostomia and keratoconjunctivitis sicca. Germinal centre-like structures (GC) are found in the minor salivary glands of approximately 25% of patients. In this study, we aimed to assess genetic variations in pSS patients with GC-like formations (GC+) compared with patients without such formations (GC−).                                

Methods Minor salivary gland biopsies from Swedish and Norwegian pSS patients (n=320) were evaluated for GC-like formations, identifying 76 GC+ and 244 GC− patients. A panel of 1536 single-nucleotide polymorphisms (SNPs) in 107 genes was genotyped. Minor allele frequencies in GC+ and GC− patients were compared using Fisher's exact test, and associations were considered significant when p<4.7×10−4 and suggestive when p<0.01.                                

Results In this case-only analysis, we identified two SNPs in CCL11 (eotaxin) associated with GC-like structures (p<4.7×10−4, OR 0.45 and 0.41, respectively). A haplotype of the two minor alleles was associated with GC status with p=2.6×10−4, OR 0.40. Suggestive associations (p<0.01) were found in SNPs in the B cell activation and/or GC-formation related genes AICDA, BANK1 and BCL2. Furthermore, SNPs in IL17A, ICA1, PKN1 and SNPs in the NF-κB pathway genes CARD8, IKBKE and TANK were found suggestively associated with GC-like structures.                                

Conclusions Our findings suggest that genetic variations may explain why ectopic GC-like structures are present in some pSS patients, and support the hypothesis that GC+ and GC− patients represent distinct disease phenotypes.

Place, publisher, year, edition, pages
B M J Group , 2014. Vol. 73, no 6, 1253-1258 p.
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-105186DOI: 10.1136/annrheumdis-2012-202500ISI: 000335362100053PubMedID: 23606706OAI: diva2:704468
Available from: 2014-03-12 Created: 2014-03-11 Last updated: 2014-11-13

Open Access in DiVA

No full text

Other links

Publisher's full textPubMed

Search in DiVA

By author/editor
Eriksson, Per
By organisation
Division of Inflammation MedicineFaculty of Health SciencesDepartment of Rheumatology
In the same journal
Annals of the Rheumatic Diseases
Medical and Health Sciences

Search outside of DiVA

GoogleGoogle Scholar
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 41 hits
ReferencesLink to record
Permanent link

Direct link