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  • Reksten, Tove RagnaUppsala universitet,Reumatologi,University of Bergen, Norway / Uppsala University, Sweden (author)

Genetic associations to germinal centre formation in primary Sjögren's syndrome

  • Article/chapterEnglish2014

Publisher, publication year, extent ...

  • 2013-04-20
  • BMJ,2014
  • printrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:uu-205113
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-205113URI
  • https://doi.org/10.1136/annrheumdis-2012-202500DOI
  • https://lup.lub.lu.se/record/4482329URI
  • https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-105186URI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:128835237URI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • BackgroundPrimary 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−).MethodsMinor 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.ResultsIn 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.ConclusionsOur 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.

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  • Johnsen, Svein Joar AuglændStavanger University Hospital, Norway (author)
  • Jonsson, Malin ViktoriaUniversity of Bergen, Norway (author)
  • Omdal, RoaldStavanger University Hospital, Norway (author)
  • Brun, Johan GUniversity of Bergen, Norway (author)
  • Theander, ElkeLund University,Lunds universitet,Internmedicin - epidemiologi,Forskargrupper vid Lunds universitet,Internal Medicine - Epidemiology,Lund University Research Groups,Skåne University Hospital, Lund University, Malmö, Sweden(Swepub:lu)medf-eth (author)
  • Eriksson, PerÖstergötlands Läns Landsting,Linköpings universitet,Avdelningen för inflammationsmedicin,Hälsouniversitetet,Reumatologiska kliniken i Östergötland(Swepub:liu)perer22 (author)
  • Wahren-Herlenius, MarieKarolinska Institutet (author)
  • Jonsson, RolandUniversity of Bergen, Norway / Haukeland University Hospital, Bergen, Norway (author)
  • Nordmark, GunnelUppsala universitet,Reumatologi,Uppsala University, Sweden(Swepub:uu)gunnnord (author)
  • Uppsala universitetReumatologi (creator_code:org_t)

Related titles

  • In:Annals of the Rheumatic Diseases: BMJ73:6, s. 1253-12580003-49671468-2060

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