Influence of the IL17A locus in giant cell arteritis susceptibility

Ana Márquez, J. Hernández-Rodríguez, M. C. Cid, R. Solans, S. Castañeda, M. E. Fernández-Contreras, M. Ramentol, I. C. Morado, J. Narváez, C. Gómez-Vaquero, V. M. Martínez-Taboada, N. Ortego-Centeno, B. Sopeña, J. Monfort, M. J. García-Villanueva, L. Caminal-Montero, E. De Miguel, R. Blanco, O. Palm, O. MolbergJ. Latus, N. Braun, F. Moosig, T. Witte, L. Beretta, A. Santaniello, G. Pazzola, L. Boiardi, C. Salvarani, M. A. González-Gay, J. Martín

Research output: Contribution to journalArticle

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Abstract

Objective: Different lines of evidence have highlighted the role of IL-17A in the inflammatory process occurring in giant cell arteritis (GCA). The aim of the present study was to assess whether the IL17A locus in fluences GCA susceptibility and its clinical subphenotypes. Methods: We carried out a large meta-analysis including a total of 1266 biopsy-proven GCA patients and 3779 healthy controls from four European populations (Spain, Italy, Germany and Norway). Five IL17A polymorphisms (rs4711998, rs8193036, rs3819024, rs2275913 and rs7747909) were selected by tagging and genotyped using TaqMan assays. Allelic combination and dependency tests were also performed. Results: In the pooled analysis, two of the five analysed polymorphisms showed evidence of association with GCA (rs2275913: PMH=1.85E-03, OR=1.17 (1.06-1.29); rs7747909: PMH=8.49E -03, OR=1.15 (1.04-1.27)). A clear trend of association was also found for the rs4711998 variant (PMH=0.059, OR=1.11 (1.00-1.23)). An independent effect of rs2275913 and rs4711998 was evident by conditional regression analysis. In addition, the haplotype harbouring the risk alleles better explained the observed association than the polymorphisms independently (likelihood p value -05). Conclusions: Polymorphisms within the IL17A locus show a novel association with GCA. This finding supports the relevant role of the Th17 cells in this vasculitis pathophysiology.

Original languageEnglish
Pages (from-to)1742-1745
Number of pages4
JournalAnnals of the Rheumatic Diseases
Volume73
Issue number9
DOIs
Publication statusPublished - 2014

Fingerprint

Giant Cell Arteritis
Polymorphism
Association reactions
Interleukin-17
Biopsy
Th17 Cells
Regression analysis
Assays
Norway
Vasculitis
Spain
Haplotypes
Italy
Germany
Meta-Analysis
Alleles
Regression Analysis
Population

ASJC Scopus subject areas

  • Rheumatology
  • Immunology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Allergy

Cite this

Márquez, A., Hernández-Rodríguez, J., Cid, M. C., Solans, R., Castañeda, S., Fernández-Contreras, M. E., ... Martín, J. (2014). Influence of the IL17A locus in giant cell arteritis susceptibility. Annals of the Rheumatic Diseases, 73(9), 1742-1745. https://doi.org/10.1136/annrheumdis-2014-205261

Influence of the IL17A locus in giant cell arteritis susceptibility. / Márquez, Ana; Hernández-Rodríguez, J.; Cid, M. C.; Solans, R.; Castañeda, S.; Fernández-Contreras, M. E.; Ramentol, M.; Morado, I. C.; Narváez, J.; Gómez-Vaquero, C.; Martínez-Taboada, V. M.; Ortego-Centeno, N.; Sopeña, B.; Monfort, J.; García-Villanueva, M. J.; Caminal-Montero, L.; De Miguel, E.; Blanco, R.; Palm, O.; Molberg, O.; Latus, J.; Braun, N.; Moosig, F.; Witte, T.; Beretta, L.; Santaniello, A.; Pazzola, G.; Boiardi, L.; Salvarani, C.; González-Gay, M. A.; Martín, J.

In: Annals of the Rheumatic Diseases, Vol. 73, No. 9, 2014, p. 1742-1745.

Research output: Contribution to journalArticle

Márquez, A, Hernández-Rodríguez, J, Cid, MC, Solans, R, Castañeda, S, Fernández-Contreras, ME, Ramentol, M, Morado, IC, Narváez, J, Gómez-Vaquero, C, Martínez-Taboada, VM, Ortego-Centeno, N, Sopeña, B, Monfort, J, García-Villanueva, MJ, Caminal-Montero, L, De Miguel, E, Blanco, R, Palm, O, Molberg, O, Latus, J, Braun, N, Moosig, F, Witte, T, Beretta, L, Santaniello, A, Pazzola, G, Boiardi, L, Salvarani, C, González-Gay, MA & Martín, J 2014, 'Influence of the IL17A locus in giant cell arteritis susceptibility', Annals of the Rheumatic Diseases, vol. 73, no. 9, pp. 1742-1745. https://doi.org/10.1136/annrheumdis-2014-205261
Márquez A, Hernández-Rodríguez J, Cid MC, Solans R, Castañeda S, Fernández-Contreras ME et al. Influence of the IL17A locus in giant cell arteritis susceptibility. Annals of the Rheumatic Diseases. 2014;73(9):1742-1745. https://doi.org/10.1136/annrheumdis-2014-205261
Márquez, Ana ; Hernández-Rodríguez, J. ; Cid, M. C. ; Solans, R. ; Castañeda, S. ; Fernández-Contreras, M. E. ; Ramentol, M. ; Morado, I. C. ; Narváez, J. ; Gómez-Vaquero, C. ; Martínez-Taboada, V. M. ; Ortego-Centeno, N. ; Sopeña, B. ; Monfort, J. ; García-Villanueva, M. J. ; Caminal-Montero, L. ; De Miguel, E. ; Blanco, R. ; Palm, O. ; Molberg, O. ; Latus, J. ; Braun, N. ; Moosig, F. ; Witte, T. ; Beretta, L. ; Santaniello, A. ; Pazzola, G. ; Boiardi, L. ; Salvarani, C. ; González-Gay, M. A. ; Martín, J. / Influence of the IL17A locus in giant cell arteritis susceptibility. In: Annals of the Rheumatic Diseases. 2014 ; Vol. 73, No. 9. pp. 1742-1745.
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abstract = "Objective: Different lines of evidence have highlighted the role of IL-17A in the inflammatory process occurring in giant cell arteritis (GCA). The aim of the present study was to assess whether the IL17A locus in fluences GCA susceptibility and its clinical subphenotypes. Methods: We carried out a large meta-analysis including a total of 1266 biopsy-proven GCA patients and 3779 healthy controls from four European populations (Spain, Italy, Germany and Norway). Five IL17A polymorphisms (rs4711998, rs8193036, rs3819024, rs2275913 and rs7747909) were selected by tagging and genotyped using TaqMan assays. Allelic combination and dependency tests were also performed. Results: In the pooled analysis, two of the five analysed polymorphisms showed evidence of association with GCA (rs2275913: PMH=1.85E-03, OR=1.17 (1.06-1.29); rs7747909: PMH=8.49E -03, OR=1.15 (1.04-1.27)). A clear trend of association was also found for the rs4711998 variant (PMH=0.059, OR=1.11 (1.00-1.23)). An independent effect of rs2275913 and rs4711998 was evident by conditional regression analysis. In addition, the haplotype harbouring the risk alleles better explained the observed association than the polymorphisms independently (likelihood p value -05). Conclusions: Polymorphisms within the IL17A locus show a novel association with GCA. This finding supports the relevant role of the Th17 cells in this vasculitis pathophysiology.",
author = "Ana M{\'a}rquez and J. Hern{\'a}ndez-Rodr{\'i}guez and Cid, {M. C.} and R. Solans and S. Casta{\~n}eda and Fern{\'a}ndez-Contreras, {M. E.} and M. Ramentol and Morado, {I. C.} and J. Narv{\'a}ez and C. G{\'o}mez-Vaquero and Mart{\'i}nez-Taboada, {V. M.} and N. Ortego-Centeno and B. Sope{\~n}a and J. Monfort and Garc{\'i}a-Villanueva, {M. J.} and L. Caminal-Montero and {De Miguel}, E. and R. Blanco and O. Palm and O. Molberg and J. Latus and N. Braun and F. Moosig and T. Witte and L. Beretta and A. Santaniello and G. Pazzola and L. Boiardi and C. Salvarani and Gonz{\'a}lez-Gay, {M. A.} and J. Mart{\'i}n",
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T1 - Influence of the IL17A locus in giant cell arteritis susceptibility

AU - Márquez, Ana

AU - Hernández-Rodríguez, J.

AU - Cid, M. C.

AU - Solans, R.

AU - Castañeda, S.

AU - Fernández-Contreras, M. E.

AU - Ramentol, M.

AU - Morado, I. C.

AU - Narváez, J.

AU - Gómez-Vaquero, C.

AU - Martínez-Taboada, V. M.

AU - Ortego-Centeno, N.

AU - Sopeña, B.

AU - Monfort, J.

AU - García-Villanueva, M. J.

AU - Caminal-Montero, L.

AU - De Miguel, E.

AU - Blanco, R.

AU - Palm, O.

AU - Molberg, O.

AU - Latus, J.

AU - Braun, N.

AU - Moosig, F.

AU - Witte, T.

AU - Beretta, L.

AU - Santaniello, A.

AU - Pazzola, G.

AU - Boiardi, L.

AU - Salvarani, C.

AU - González-Gay, M. A.

AU - Martín, J.

PY - 2014

Y1 - 2014

N2 - Objective: Different lines of evidence have highlighted the role of IL-17A in the inflammatory process occurring in giant cell arteritis (GCA). The aim of the present study was to assess whether the IL17A locus in fluences GCA susceptibility and its clinical subphenotypes. Methods: We carried out a large meta-analysis including a total of 1266 biopsy-proven GCA patients and 3779 healthy controls from four European populations (Spain, Italy, Germany and Norway). Five IL17A polymorphisms (rs4711998, rs8193036, rs3819024, rs2275913 and rs7747909) were selected by tagging and genotyped using TaqMan assays. Allelic combination and dependency tests were also performed. Results: In the pooled analysis, two of the five analysed polymorphisms showed evidence of association with GCA (rs2275913: PMH=1.85E-03, OR=1.17 (1.06-1.29); rs7747909: PMH=8.49E -03, OR=1.15 (1.04-1.27)). A clear trend of association was also found for the rs4711998 variant (PMH=0.059, OR=1.11 (1.00-1.23)). An independent effect of rs2275913 and rs4711998 was evident by conditional regression analysis. In addition, the haplotype harbouring the risk alleles better explained the observed association than the polymorphisms independently (likelihood p value -05). Conclusions: Polymorphisms within the IL17A locus show a novel association with GCA. This finding supports the relevant role of the Th17 cells in this vasculitis pathophysiology.

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