Abstract
Recent reports have proven the importance of genetic factors and inflammation in the pathogenesis of rheumatoid arthritis (RA). In the current study, the frequency of NOD2/CARD15 gene variants (R702W, G908R, and L1007fsinsC) was examined in a group of 243 RA patients and 220 healthy controls. There were no statistically significant differences in distribution of NOD2 variant alleles between RA patients and controls. Moreover, there was no significant association between NOD2 variant alleles and joint erosions, extraarticular manifestations, rheumatoid factor, number of swollen and tender joints, and erythrocyte sedimentation rate. The results of the present study suggest that NOD2 allele variants have no significant influence on RA susceptibility, activity, and severity.
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Reveille JD (1998) The genetic contribution to the pathogenesis of rheumatoid arthritis. Curr Opin Rheumatol 10:187–200
Kaltschmidt B, Baeuerle PA, Kaltschmidt C (1993) Potential involvement of the transcription factor NF-kappa B in neurological disorders. Mol Aspects Med 14:171–190
Inohara N, Nunez G (2003) NODs: intracellular proteins involved in inflammation and apoptosis. Nat Rev Immunol 3:371–382
Ogura Y, Bonen DK, Inohara N, Nicolae DL, Chen FF, Ramos R et al (2001) A frameshift mutation in NOD2 associated with susceptibility to Crohn’s disease. Nature 411:603–606
Kurzawski G, Suchy J, Kladny J, Grabowska E, Mierzejewski M, Jakubowska A et al (2004) The NOD2 3020insC mutation and the risk of colorectal cancer. Cancer Res 64:1604–1606
Maeda S, Hsu LC, Liu H, Bankston LA, Iimura M, Kagnoff MF et al (2005) Nod2 mutation in Crohn’s disease potentiates NF-kappaB activity and IL-1beta processing. Science 307:734–738
Prevoo ML, van’t Hof MA, Kuper HH, van Leeuwen MA, van de Putte LB, van Riel PL (1995) Modified disease activity scores that include twenty-eight-joint counts. Development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. Arthritis Rheum 38:44–48
Felson DT, Anderson JJ, Boers M, Bombardier C, Chernoff M, Fried B et al (1993) The American College of Rheumatology preliminary core set of disease activity measures for rheumatoid arthritis clinical trials. The committee on outcome measures in rheumatoid arthritis clinical trials. Arthritis Rheum 36:729–740
Lesage S, Zouali H, Cezard JP, Colombel JF, Belaiche J, Almer S et al (2002) CARD15/NOD2 mutational analysis and genotype-phenotype correlation in 612 patients with inflammatory bowel disease. Am J Hum Genet 70:845–857
Ferreiros-Vidal I, Barros F, Pablos JL, Carracedo A, Gomez-Reino JJ, Gonzalez A (2003) CARD15/NOD2 analysis in rheumatoid arthritis susceptibility. Rheumatol (Oxf) 42:1380–1382
Steer S, Fisher SA, Fife M, Cuthbert A, Newton J, Wordsworth P et al (2003) Development of rheumatoid arthritis is not associated with two polymorphisms in the Crohn’s disease gene CARD15. Rheumatol (Oxf) 42:304–307
Collantes E, Valle Blazquez M, Mazorra V, Macho A, Aranda E, Munoz E (1998) Nuclear factor-kappa B activity in T cells from patients with rheumatic diseases: a preliminary report. Ann Rheum Dis 57:738–741
Gerlag DM, Ransone L, Tak PP, Han Z, Palanki M, Barbosa MS et al (2000) The effect of a T cell-specific NF-kappa B inhibitor on in vitro cytokine production and collagen-induced arthritis. J Immunol 165:1652–1658
McInnes IB, Leung BP, Sturrock RD, Field M, Liew FY (1997) Interleukin-15 mediates T cell-dependent regulation of tumor necrosis factor-alpha production in rheumatoid arthritis. Nat Med 3:189–195
Tak PP, Gerlag DM, Aupperle KR, van de Geest DA, Overbeek M, Bennett BL et al (2001) Inhibitor of nuclear factor kappaB kinase beta is a key regulator of synovial inflammation. Arthritis Rheum 44:1897–1907
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Pawlik, A., Kurzawski, M., Gawronska-Szklarz, B. et al. NOD2 allele variants in patients with rheumatoid arthritis. Clin Rheumatol 26, 868–871 (2007). https://doi.org/10.1007/s10067-006-0404-1
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DOI: https://doi.org/10.1007/s10067-006-0404-1