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STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis
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| Zeitschriftentitel: | Arthritis & Rheumatism |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , , , , , , , , , , |
| In: | Arthritis & Rheumatism, 60, 2009, 8, S. 2472-2479 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
Dieudé, P. Guedj, M. Wipff, J. Ruiz, B. Hachulla, E. Diot, E. Granel, B. Sibilia, J. Tiev, K. Mouthon, L. Cracowski, J.L. Carpentier, P.H. Amoura, Z. Fajardy, I. Avouac, J. Meyer, O. Kahan, A. Boileau, C. Allanore, Y. Dieudé, P. Guedj, M. Wipff, J. Ruiz, B. Hachulla, E. Diot, E. Granel, B. Sibilia, J. Tiev, K. Mouthon, L. Cracowski, J.L. Carpentier, P.H. Amoura, Z. Fajardy, I. Avouac, J. Meyer, O. Kahan, A. Boileau, C. Allanore, Y. |
|---|---|
| author |
Dieudé, P. Guedj, M. Wipff, J. Ruiz, B. Hachulla, E. Diot, E. Granel, B. Sibilia, J. Tiev, K. Mouthon, L. Cracowski, J.L. Carpentier, P.H. Amoura, Z. Fajardy, I. Avouac, J. Meyer, O. Kahan, A. Boileau, C. Allanore, Y. |
| spellingShingle |
Dieudé, P. Guedj, M. Wipff, J. Ruiz, B. Hachulla, E. Diot, E. Granel, B. Sibilia, J. Tiev, K. Mouthon, L. Cracowski, J.L. Carpentier, P.H. Amoura, Z. Fajardy, I. Avouac, J. Meyer, O. Kahan, A. Boileau, C. Allanore, Y. Arthritis & Rheumatism STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis Pharmacology (medical) Immunology Rheumatology Immunology and Allergy |
| author_sort |
dieudé, p. |
| spelling |
Dieudé, P. Guedj, M. Wipff, J. Ruiz, B. Hachulla, E. Diot, E. Granel, B. Sibilia, J. Tiev, K. Mouthon, L. Cracowski, J.L. Carpentier, P.H. Amoura, Z. Fajardy, I. Avouac, J. Meyer, O. Kahan, A. Boileau, C. Allanore, Y. 0004-3591 1529-0131 Wiley Pharmacology (medical) Immunology Rheumatology Immunology and Allergy http://dx.doi.org/10.1002/art.24688 <jats:title>Abstract</jats:title><jats:sec><jats:title>Objective</jats:title><jats:p>Systemic sclerosis (SSc) belongs to the group of connective tissue disorders (CTDs), among which are several disorders characterized by a type I interferon (IFN) signature. The recent identification of an association between <jats:italic>IRF5</jats:italic> and SSc further highlights a key role for IFN. <jats:italic>STAT4</jats:italic>, which encodes STAT‐4, contributes to IFN signaling, and its genetic variants were found to be associated with CTDs. The aim of this study was to determine whether the <jats:italic>STAT4</jats:italic> rs7574865 single‐nucleotide polymorphism is associated with SSc, and whether it interacts with <jats:italic>IRF5</jats:italic>.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Both the <jats:italic>STAT4</jats:italic> rs7574865 and <jats:italic>IRF5</jats:italic> rs2004640 polymorphisms were genotyped in 1,855 individuals of French Caucasian origin comprising a discovery set of 440 patients with SSc and 485 control subjects and a replication set of 445 patients with SSc and an additional 485 control subjects.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:italic>STAT4</jats:italic> rs7574865 was shown to be associated with SSc (<jats:italic>P</jats:italic> = 0.001, odds ratio [OR] 1.29, 95% confidence interval [95% CI] 1.11–1.51). This association was not restricted to a particular phenotype. An additive effect of the <jats:italic>STAT4</jats:italic> rs7574865 T allele and the <jats:italic>IRF5</jats:italic> rs2004640 T allele was observed, resulting in a multiplicatively increased 1.28‐fold risk of SSc. The OR for SSc was 2.72 (95% CI 1.86–3.99) for combinations of genotypes with ≥3 risk alleles. An additive effect was also detected for fibrosing alveolitis: carriage of at least 3 risk alleles appeared to be an independent risk factor (<jats:italic>P</jats:italic> = 2.2 × 10<jats:sup>−4</jats:sup>, OR 1.97, 95% CI 1.28–3.04).</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Our results establish <jats:italic>STAT4</jats:italic> rs7574865 as a new SSc genetic susceptibility factor. <jats:italic>STAT4</jats:italic> and <jats:italic>IRF5</jats:italic> act with additive effects in terms of susceptibility to both SSc and SSc‐related fibrosing alveolitis.</jats:p></jats:sec> <i>STAT4</i> is a genetic risk factor for systemic sclerosis having additive effects with <i>IRF5</i> on disease susceptibility and related pulmonary fibrosis Arthritis & Rheumatism |
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10.1002/art.24688 |
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Chemie und Pharmazie Medizin |
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Wiley, 2009 |
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Wiley, 2009 |
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1529-0131 0004-3591 |
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dieude2009stat4isageneticriskfactorforsystemicsclerosishavingadditiveeffectswithirf5ondiseasesusceptibilityandrelatedpulmonaryfibrosis |
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2009 |
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Arthritis & Rheumatism |
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49 |
| title |
STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis |
| title_unstemmed |
STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis |
| title_full |
STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis |
| title_fullStr |
STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis |
| title_full_unstemmed |
STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis |
| title_short |
STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis |
| title_sort |
<i>stat4</i> is a genetic risk factor for systemic sclerosis having additive effects with <i>irf5</i> on disease susceptibility and related pulmonary fibrosis |
| topic |
Pharmacology (medical) Immunology Rheumatology Immunology and Allergy |
| url |
http://dx.doi.org/10.1002/art.24688 |
| publishDate |
2009 |
| physical |
2472-2479 |
| description |
<jats:title>Abstract</jats:title><jats:sec><jats:title>Objective</jats:title><jats:p>Systemic sclerosis (SSc) belongs to the group of connective tissue disorders (CTDs), among which are several disorders characterized by a type I interferon (IFN) signature. The recent identification of an association between <jats:italic>IRF5</jats:italic> and SSc further highlights a key role for IFN. <jats:italic>STAT4</jats:italic>, which encodes STAT‐4, contributes to IFN signaling, and its genetic variants were found to be associated with CTDs. The aim of this study was to determine whether the <jats:italic>STAT4</jats:italic> rs7574865 single‐nucleotide polymorphism is associated with SSc, and whether it interacts with <jats:italic>IRF5</jats:italic>.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Both the <jats:italic>STAT4</jats:italic> rs7574865 and <jats:italic>IRF5</jats:italic> rs2004640 polymorphisms were genotyped in 1,855 individuals of French Caucasian origin comprising a discovery set of 440 patients with SSc and 485 control subjects and a replication set of 445 patients with SSc and an additional 485 control subjects.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:italic>STAT4</jats:italic> rs7574865 was shown to be associated with SSc (<jats:italic>P</jats:italic> = 0.001, odds ratio [OR] 1.29, 95% confidence interval [95% CI] 1.11–1.51). This association was not restricted to a particular phenotype. An additive effect of the <jats:italic>STAT4</jats:italic> rs7574865 T allele and the <jats:italic>IRF5</jats:italic> rs2004640 T allele was observed, resulting in a multiplicatively increased 1.28‐fold risk of SSc. The OR for SSc was 2.72 (95% CI 1.86–3.99) for combinations of genotypes with ≥3 risk alleles. An additive effect was also detected for fibrosing alveolitis: carriage of at least 3 risk alleles appeared to be an independent risk factor (<jats:italic>P</jats:italic> = 2.2 × 10<jats:sup>−4</jats:sup>, OR 1.97, 95% CI 1.28–3.04).</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Our results establish <jats:italic>STAT4</jats:italic> rs7574865 as a new SSc genetic susceptibility factor. <jats:italic>STAT4</jats:italic> and <jats:italic>IRF5</jats:italic> act with additive effects in terms of susceptibility to both SSc and SSc‐related fibrosing alveolitis.</jats:p></jats:sec> |
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| author | Dieudé, P., Guedj, M., Wipff, J., Ruiz, B., Hachulla, E., Diot, E., Granel, B., Sibilia, J., Tiev, K., Mouthon, L., Cracowski, J.L., Carpentier, P.H., Amoura, Z., Fajardy, I., Avouac, J., Meyer, O., Kahan, A., Boileau, C., Allanore, Y. |
| author_facet | Dieudé, P., Guedj, M., Wipff, J., Ruiz, B., Hachulla, E., Diot, E., Granel, B., Sibilia, J., Tiev, K., Mouthon, L., Cracowski, J.L., Carpentier, P.H., Amoura, Z., Fajardy, I., Avouac, J., Meyer, O., Kahan, A., Boileau, C., Allanore, Y., Dieudé, P., Guedj, M., Wipff, J., Ruiz, B., Hachulla, E., Diot, E., Granel, B., Sibilia, J., Tiev, K., Mouthon, L., Cracowski, J.L., Carpentier, P.H., Amoura, Z., Fajardy, I., Avouac, J., Meyer, O., Kahan, A., Boileau, C., Allanore, Y. |
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| description | <jats:title>Abstract</jats:title><jats:sec><jats:title>Objective</jats:title><jats:p>Systemic sclerosis (SSc) belongs to the group of connective tissue disorders (CTDs), among which are several disorders characterized by a type I interferon (IFN) signature. The recent identification of an association between <jats:italic>IRF5</jats:italic> and SSc further highlights a key role for IFN. <jats:italic>STAT4</jats:italic>, which encodes STAT‐4, contributes to IFN signaling, and its genetic variants were found to be associated with CTDs. The aim of this study was to determine whether the <jats:italic>STAT4</jats:italic> rs7574865 single‐nucleotide polymorphism is associated with SSc, and whether it interacts with <jats:italic>IRF5</jats:italic>.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Both the <jats:italic>STAT4</jats:italic> rs7574865 and <jats:italic>IRF5</jats:italic> rs2004640 polymorphisms were genotyped in 1,855 individuals of French Caucasian origin comprising a discovery set of 440 patients with SSc and 485 control subjects and a replication set of 445 patients with SSc and an additional 485 control subjects.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:italic>STAT4</jats:italic> rs7574865 was shown to be associated with SSc (<jats:italic>P</jats:italic> = 0.001, odds ratio [OR] 1.29, 95% confidence interval [95% CI] 1.11–1.51). This association was not restricted to a particular phenotype. An additive effect of the <jats:italic>STAT4</jats:italic> rs7574865 T allele and the <jats:italic>IRF5</jats:italic> rs2004640 T allele was observed, resulting in a multiplicatively increased 1.28‐fold risk of SSc. The OR for SSc was 2.72 (95% CI 1.86–3.99) for combinations of genotypes with ≥3 risk alleles. An additive effect was also detected for fibrosing alveolitis: carriage of at least 3 risk alleles appeared to be an independent risk factor (<jats:italic>P</jats:italic> = 2.2 × 10<jats:sup>−4</jats:sup>, OR 1.97, 95% CI 1.28–3.04).</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Our results establish <jats:italic>STAT4</jats:italic> rs7574865 as a new SSc genetic susceptibility factor. <jats:italic>STAT4</jats:italic> and <jats:italic>IRF5</jats:italic> act with additive effects in terms of susceptibility to both SSc and SSc‐related fibrosing alveolitis.</jats:p></jats:sec> |
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| spelling | Dieudé, P. Guedj, M. Wipff, J. Ruiz, B. Hachulla, E. Diot, E. Granel, B. Sibilia, J. Tiev, K. Mouthon, L. Cracowski, J.L. Carpentier, P.H. Amoura, Z. Fajardy, I. Avouac, J. Meyer, O. Kahan, A. Boileau, C. Allanore, Y. 0004-3591 1529-0131 Wiley Pharmacology (medical) Immunology Rheumatology Immunology and Allergy http://dx.doi.org/10.1002/art.24688 <jats:title>Abstract</jats:title><jats:sec><jats:title>Objective</jats:title><jats:p>Systemic sclerosis (SSc) belongs to the group of connective tissue disorders (CTDs), among which are several disorders characterized by a type I interferon (IFN) signature. The recent identification of an association between <jats:italic>IRF5</jats:italic> and SSc further highlights a key role for IFN. <jats:italic>STAT4</jats:italic>, which encodes STAT‐4, contributes to IFN signaling, and its genetic variants were found to be associated with CTDs. The aim of this study was to determine whether the <jats:italic>STAT4</jats:italic> rs7574865 single‐nucleotide polymorphism is associated with SSc, and whether it interacts with <jats:italic>IRF5</jats:italic>.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Both the <jats:italic>STAT4</jats:italic> rs7574865 and <jats:italic>IRF5</jats:italic> rs2004640 polymorphisms were genotyped in 1,855 individuals of French Caucasian origin comprising a discovery set of 440 patients with SSc and 485 control subjects and a replication set of 445 patients with SSc and an additional 485 control subjects.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:italic>STAT4</jats:italic> rs7574865 was shown to be associated with SSc (<jats:italic>P</jats:italic> = 0.001, odds ratio [OR] 1.29, 95% confidence interval [95% CI] 1.11–1.51). This association was not restricted to a particular phenotype. An additive effect of the <jats:italic>STAT4</jats:italic> rs7574865 T allele and the <jats:italic>IRF5</jats:italic> rs2004640 T allele was observed, resulting in a multiplicatively increased 1.28‐fold risk of SSc. The OR for SSc was 2.72 (95% CI 1.86–3.99) for combinations of genotypes with ≥3 risk alleles. An additive effect was also detected for fibrosing alveolitis: carriage of at least 3 risk alleles appeared to be an independent risk factor (<jats:italic>P</jats:italic> = 2.2 × 10<jats:sup>−4</jats:sup>, OR 1.97, 95% CI 1.28–3.04).</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Our results establish <jats:italic>STAT4</jats:italic> rs7574865 as a new SSc genetic susceptibility factor. <jats:italic>STAT4</jats:italic> and <jats:italic>IRF5</jats:italic> act with additive effects in terms of susceptibility to both SSc and SSc‐related fibrosing alveolitis.</jats:p></jats:sec> <i>STAT4</i> is a genetic risk factor for systemic sclerosis having additive effects with <i>IRF5</i> on disease susceptibility and related pulmonary fibrosis Arthritis & Rheumatism |
| spellingShingle | Dieudé, P., Guedj, M., Wipff, J., Ruiz, B., Hachulla, E., Diot, E., Granel, B., Sibilia, J., Tiev, K., Mouthon, L., Cracowski, J.L., Carpentier, P.H., Amoura, Z., Fajardy, I., Avouac, J., Meyer, O., Kahan, A., Boileau, C., Allanore, Y., Arthritis & Rheumatism, STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis, Pharmacology (medical), Immunology, Rheumatology, Immunology and Allergy |
| title | STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis |
| title_full | STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis |
| title_fullStr | STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis |
| title_full_unstemmed | STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis |
| title_short | STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis |
| title_sort | <i>stat4</i> is a genetic risk factor for systemic sclerosis having additive effects with <i>irf5</i> on disease susceptibility and related pulmonary fibrosis |
| title_unstemmed | STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis |
| topic | Pharmacology (medical), Immunology, Rheumatology, Immunology and Allergy |
| url | http://dx.doi.org/10.1002/art.24688 |