Polymorphisms in the interferon-gamma/interleukin-26 gene region contribute to sex bias in susceptibility to rheumatoid arthritis - PubMed (original) (raw)
. 2003 Oct;48(10):2773-8.
doi: 10.1002/art.11236.
Affiliations
- PMID: 14558082
- DOI: 10.1002/art.11236
Free article
Polymorphisms in the interferon-gamma/interleukin-26 gene region contribute to sex bias in susceptibility to rheumatoid arthritis
K Vandenbroeck et al. Arthritis Rheum. 2003 Oct.
Free article
Abstract
Objective: To determine whether polymorphisms in the interferon-gamma (IFNgamma)/interleukin-26 (IL-26; formerly, AK155) gene cluster contribute to sex-based differential susceptibility to rheumatoid arthritis (RA).
Methods: Four microsatellite markers, located in a 118-kb interval that contains both the IFNgamma and IL-26 genes on chromosome 12q15, were typed in 251 patients with RA and 198 unrelated healthy controls (all of whom lived in Northern Ireland) by means of polymerase chain reaction-based fragment analysis.
Results: Marker D12S2510, which is located 3 kb 3' from the IL-26 gene, was significantly associated with RA in women (corrected P [P(corr)] = 0.008, 2 degrees of freedom [2 df]) but not in men (P = 0.99, 2 df). A 3-marker haplotype, IFNGCA*13;D12S2510*8;D12S2511*9, was inferred that showed significant underrepresentation in women with RA (odds ratio 0.50, 95% confidence interval 0.32-0.78; P = 0.002, P(corr) = 0.03) but not in men with RA.
Conclusion: Our results demonstrate that common polymorphisms in the IFNgamma/IL-26 gene region may contribute to sex bias in susceptibility to RA, by distorting the propensity of female carriers versus male carriers to contract this disease. These results conform to our recent observations of a role for this gene cluster in sex-based differential susceptibility to another Th1-type inflammatory disease, multiple sclerosis.
Similar articles
- Association of arthritis with a gene complex encoding C-type lectin-like receptors.
Lorentzen JC, Flornes L, Eklöw C, Bäckdahl L, Ribbhammar U, Guo JP, Smolnikova M, Dissen E, Seddighzadeh M, Brookes AJ, Alfredsson L, Klareskog L, Padyukov L, Fossum S. Lorentzen JC, et al. Arthritis Rheum. 2007 Aug;56(8):2620-32. doi: 10.1002/art.22813. Arthritis Rheum. 2007. PMID: 17665455 - Interferon gamma allelic variants: sex-biased multiple sclerosis susceptibility and gene expression.
Kantarci OH, Hebrink DD, Schaefer-Klein J, Sun Y, Achenbach S, Atkinson EJ, Heggarty S, Cotleur AC, de Andrade M, Vandenbroeck K, Pelfrey CM, Weinshenker BG. Kantarci OH, et al. Arch Neurol. 2008 Mar;65(3):349-57. doi: 10.1001/archneurol.2007.66. Arch Neurol. 2008. PMID: 18332247 - A poly(ADP-ribose) polymerase haplotype spanning the promoter region confers susceptibility to rheumatoid arthritis.
Pascual M, López-Nevot MA, Cáliz R, Ferrer MA, Balsa A, Pascual-Salcedo D, Martín J. Pascual M, et al. Arthritis Rheum. 2003 Mar;48(3):638-41. doi: 10.1002/art.10864. Arthritis Rheum. 2003. PMID: 12632415 - Interleukin-18 gene (IL18) promoter polymorphisms in patients with rheumatoid arthritis.
Pawlik A, Kurzawski M, Drozdzik M, Dziedziejko V, Safranow K, Herczynska M. Pawlik A, et al. Scand J Rheumatol. 2009 May-Jun;38(3):159-65. doi: 10.1080/03009740802600748. Scand J Rheumatol. 2009. PMID: 19229765 - [Genetic testing and gene-based testing forAllergic disorders].
Kondo N, Nagaya S, Kuwabara M, Matsui E. Kondo N, et al. Nihon Rinsho. 2005 Dec;63 Suppl 12:232-9. Nihon Rinsho. 2005. PMID: 16416800 Review. Japanese. No abstract available.
Cited by
- T(H)17 cells promote microbial killing and innate immune sensing of DNA via interleukin 26.
Meller S, Di Domizio J, Voo KS, Friedrich HC, Chamilos G, Ganguly D, Conrad C, Gregorio J, Le Roy D, Roger T, Ladbury JE, Homey B, Watowich S, Modlin RL, Kontoyiannis DP, Liu YJ, Arold ST, Gilliet M. Meller S, et al. Nat Immunol. 2015 Sep;16(9):970-9. doi: 10.1038/ni.3211. Epub 2015 Jul 13. Nat Immunol. 2015. PMID: 26168081 Free PMC article. - Polymorphisms within the human leucocyte antigen-E gene and their associations with susceptibility to rheumatoid arthritis as well as clinical outcome of anti-tumour necrosis factor therapy.
Iwaszko M, Świerkot J, Kolossa K, Jeka S, Wiland P, Bogunia-Kubik K. Iwaszko M, et al. Clin Exp Immunol. 2015 Dec;182(3):270-7. doi: 10.1111/cei.12696. Epub 2015 Sep 28. Clin Exp Immunol. 2015. PMID: 26307125 Free PMC article. Clinical Trial. - IL-26, a Cytokine With Roles in Extracellular DNA-Induced Inflammation and Microbial Defense.
Larochette V, Miot C, Poli C, Beaumont E, Roingeard P, Fickenscher H, Jeannin P, Delneste Y. Larochette V, et al. Front Immunol. 2019 Feb 12;10:204. doi: 10.3389/fimmu.2019.00204. eCollection 2019. Front Immunol. 2019. PMID: 30809226 Free PMC article. Review. - Inverted expression profiles of sex-biased genes in response to toxicant perturbations and diseases.
Ung CY, Lam SH, Zhang X, Li H, Zhang L, Li B, Gong Z. Ung CY, et al. PLoS One. 2013;8(2):e56668. doi: 10.1371/journal.pone.0056668. Epub 2013 Feb 14. PLoS One. 2013. PMID: 23457601 Free PMC article. - Sex-specific exposures and sex-combined outcomes in two-sample Mendelian randomization may mislead the causal inference.
Wang Z, Lu J. Wang Z, et al. Arthritis Res Ther. 2022 Oct 24;24(1):237. doi: 10.1186/s13075-022-02922-7. Arthritis Res Ther. 2022. PMID: 36280857 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical
Molecular Biology Databases
Miscellaneous