Inflammation Research

, Volume 62, Issue 2, pp 195–200 | Cite as

Difference of interleukin-23 receptor gene haplotype variants in ulcerative colitis compared to Crohn’s disease and psoriasis

  • Eniko Safrany
  • Melinda Szabo
  • Marta Szell
  • Lajos Kemeny
  • Katalin Sumegi
  • Bela I. Melegh
  • Lili Magyari
  • Petra Matyas
  • Maria Figler
  • Agnes Weber
  • Zsolt Tulassay
  • Bela Melegh
Original Research Paper



Polymorphisms of the interleukin-23 receptor (IL23R) gene have been found to play a role in the development of several autoimmune diseases. Our aim was to examine the possible effect of not only simple individual variants, but of haplotypes composed of them.


We analysed 263 patients with psoriasis, 199 patients with Crohn’s disease (CD), 282 patients with ulcerative colitis (UC), and 253 controls for rs1884444, rs11805303, rs7517847, rs2201841, rs10889677 and rs11209032 variants.


The genotypes were determined by using PCR/RFLP assay. Logistic regression analysis was used to compare the genotype distribution of the polymorphisms and haplotypes between the examined autoimmune diseases and healthy controls.


Rs1884444 was found to confer risk for UC and psoriasis, rs10889677 for CD and psoriasis, while rs2201841 and rs7517847 had effect only in CD. Using these SNPs we could study the susceptibility haplotype profiles in these diseases with special attention to UC. Eight different haplotypes could be differentiated. We found that the SNPs exert their susceptibility character in specific haplotype blocks, and the frequency of one haplotype differed significantly in UC compared with both other diseases and also with healthy controls. This haplotype conferred risk for UC, even while it had a somewhat lower frequency in the other diseases than in controls.


The data presented here serve as evidence for the need of haplotype analysis instead of just single standing SNP analysis when susceptibility is interpreted.


IL23R Ulcerative colitis Crohn’s disease Psoriasis IBD 



This work was supported by the grant of Hungarian Science Foundation OTKA T73430 and K103983.


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Copyright information

© Springer Basel 2012

Authors and Affiliations

  • Eniko Safrany
    • 1
    • 8
  • Melinda Szabo
    • 2
  • Marta Szell
    • 3
    • 4
  • Lajos Kemeny
    • 3
    • 4
  • Katalin Sumegi
    • 1
    • 8
  • Bela I. Melegh
    • 1
    • 8
  • Lili Magyari
    • 1
    • 8
  • Petra Matyas
    • 1
    • 8
  • Maria Figler
    • 5
  • Agnes Weber
    • 6
  • Zsolt Tulassay
    • 7
  • Bela Melegh
    • 1
    • 8
  1. 1.Department of Medical GeneticsUniversity of PecsPecsHungary
  2. 2.Robert Koch HospitalEdelenyHungary
  3. 3.Dermatological Research Group of the Hungarian Academy of SciencesUniversity of SzegedSzegedHungary
  4. 4.Department of Dermatology and AllergologyUniversity of SzegedSzegedHungary
  5. 5.Second Department and Nephrological CentreUniversity of PecsPecsHungary
  6. 6.BAZ County Hospital and University Teaching HospitalMiskolcHungary
  7. 7.2nd Department of Internal MedicineSemmelweis UniversityBudapestHungary
  8. 8.Szentagothai Research CenterPecsHungary

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