A TNFSF13B functional variant is not involved in systemic sclerosis and giant cell arteritis susceptibility
The TNFSF13B (TNF superfamily member 13b) gene encodes BAFF, a cytokine with a crucial role in the differentiation and activation of B cells. An insertion-deletion variant (GCTGT→A) of this gene, leading to increased levels of BAFF, has been recently implicated in the genetic predisposition to sever...
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| Published in | PloS one Vol. 13; no. 12; p. e0209343 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
26.12.2018
Public Library of Science (PLoS) |
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| Abstract | The TNFSF13B (TNF superfamily member 13b) gene encodes BAFF, a cytokine with a crucial role in the differentiation and activation of B cells. An insertion-deletion variant (GCTGT→A) of this gene, leading to increased levels of BAFF, has been recently implicated in the genetic predisposition to several autoimmune diseases, including multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis. Based on the elevated levels of this cytokine found in patients with giant cell arteritis (GCA) and systemic sclerosis (SSc), we aimed to assess whether this functional variant also represents a novel genetic risk factor for these two disorders.
A total of 1,728 biopsy-proven GCA patients from 4 European cohorts, 4,584 SSc patients from 3 European cohorts and 5,160 ethnically-matched healthy controls were included in the study. The single nucleotide polymorphism (SNP) rs374039502, which colocalizes with the genetic variant previously implicated in autoimmunity, was genotyped using a custom TaqMan assay. First, association analysis was conducted in each independent cohort using χ2 test in Plink (v1.9). Subsequently, different case/control sets were meta-analyzed by the inverse variance method.
No statistically significant differences were found when allele distributions were compared between cases and controls for any of the analyzed cohorts. Similarly, combined analysis of the different sets evidenced a lack of association of the rs374039502 variant with GCA (P = 0.421; OR (95% CI) = 0.92 (0.75-1.13)) and SSc (P = 0.500; OR (95% CI) = 1.05 (0.91-1.22)). The stratified analysis considering the main clinical subphenotypes of these diseases yielded similar negative results.
Our data suggest that the TNFSF13B functional variant does not contribute to the genetic network underlying GCA and SSc. |
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| AbstractList | The TNFSF13B (TNF superfamily member 13b) gene encodes BAFF, a cytokine with a crucial role in the differentiation and activation of B cells. An insertion-deletion variant (GCTGT[right arrow]A) of this gene, leading to increased levels of BAFF, has been recently implicated in the genetic predisposition to several autoimmune diseases, including multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis. Based on the elevated levels of this cytokine found in patients with giant cell arteritis (GCA) and systemic sclerosis (SSc), we aimed to assess whether this functional variant also represents a novel genetic risk factor for these two disorders. A total of 1,728 biopsy-proven GCA patients from 4 European cohorts, 4,584 SSc patients from 3 European cohorts and 5,160 ethnically-matched healthy controls were included in the study. The single nucleotide polymorphism (SNP) rs374039502, which colocalizes with the genetic variant previously implicated in autoimmunity, was genotyped using a custom TaqMan assay. First, association analysis was conducted in each independent cohort using X2 test in Plink (v1.9). Subsequently, different case/control sets were meta-analyzed by the inverse variance method. No statistically significant differences were found when allele distributions were compared between cases and controls for any of the analyzed cohorts. Similarly, combined analysis of the different sets evidenced a lack of association of the rs374039502 variant with GCA (P = 0.421; OR (95% CI) = 0.92 (0.75-1.13)) and SSc (P = 0.500; OR (95% CI) = 1.05 (0.91-1.22)). The stratified analysis considering the main clinical subphenotypes of these diseases yielded similar negative results. Our data suggest that the TNFSF13B functional variant does not contribute to the genetic network underlying GCA and SSc. Background The TNFSF13B (TNF superfamily member 13b) gene encodes BAFF, a cytokine with a crucial role in the differentiation and activation of B cells. An insertion-deletion variant (GCTGT→A) of this gene, leading to increased levels of BAFF, has been recently implicated in the genetic predisposition to several autoimmune diseases, including multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis. Based on the elevated levels of this cytokine found in patients with giant cell arteritis (GCA) and systemic sclerosis (SSc), we aimed to assess whether this functional variant also represents a novel genetic risk factor for these two disorders. Methods A total of 1,728 biopsy-proven GCA patients from 4 European cohorts, 4,584 SSc patients from 3 European cohorts and 5,160 ethnically-matched healthy controls were included in the study. The single nucleotide polymorphism (SNP) rs374039502, which colocalizes with the genetic variant previously implicated in autoimmunity, was genotyped using a custom TaqMan assay. First, association analysis was conducted in each independent cohort using χ2 test in Plink (v1.9). Subsequently, different case/control sets were meta-analyzed by the inverse variance method. Results No statistically significant differences were found when allele distributions were compared between cases and controls for any of the analyzed cohorts. Similarly, combined analysis of the different sets evidenced a lack of association of the rs374039502 variant with GCA (P = 0.421; OR (95% CI) = 0.92 (0.75–1.13)) and SSc (P = 0.500; OR (95% CI) = 1.05 (0.91–1.22)). The stratified analysis considering the main clinical subphenotypes of these diseases yielded similar negative results. Conclusion Our data suggest that the TNFSF13B functional variant does not contribute to the genetic network underlying GCA and SSc. BackgroundThe TNFSF13B (TNF superfamily member 13b) gene encodes BAFF, a cytokine with a crucial role in the differentiation and activation of B cells. An insertion-deletion variant (GCTGT→A) of this gene, leading to increased levels of BAFF, has been recently implicated in the genetic predisposition to several autoimmune diseases, including multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis. Based on the elevated levels of this cytokine found in patients with giant cell arteritis (GCA) and systemic sclerosis (SSc), we aimed to assess whether this functional variant also represents a novel genetic risk factor for these two disorders.MethodsA total of 1,728 biopsy-proven GCA patients from 4 European cohorts, 4,584 SSc patients from 3 European cohorts and 5,160 ethnically-matched healthy controls were included in the study. The single nucleotide polymorphism (SNP) rs374039502, which colocalizes with the genetic variant previously implicated in autoimmunity, was genotyped using a custom TaqMan assay. First, association analysis was conducted in each independent cohort using χ2 test in Plink (v1.9). Subsequently, different case/control sets were meta-analyzed by the inverse variance method.ResultsNo statistically significant differences were found when allele distributions were compared between cases and controls for any of the analyzed cohorts. Similarly, combined analysis of the different sets evidenced a lack of association of the rs374039502 variant with GCA (P = 0.421; OR (95% CI) = 0.92 (0.75-1.13)) and SSc (P = 0.500; OR (95% CI) = 1.05 (0.91-1.22)). The stratified analysis considering the main clinical subphenotypes of these diseases yielded similar negative results.ConclusionOur data suggest that the TNFSF13B functional variant does not contribute to the genetic network underlying GCA and SSc. Background The TNFSF13B (TNF superfamily member 13b) gene encodes BAFF, a cytokine with a crucial role in the differentiation and activation of B cells. An insertion-deletion variant (GCTGT[right arrow]A) of this gene, leading to increased levels of BAFF, has been recently implicated in the genetic predisposition to several autoimmune diseases, including multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis. Based on the elevated levels of this cytokine found in patients with giant cell arteritis (GCA) and systemic sclerosis (SSc), we aimed to assess whether this functional variant also represents a novel genetic risk factor for these two disorders. Methods A total of 1,728 biopsy-proven GCA patients from 4 European cohorts, 4,584 SSc patients from 3 European cohorts and 5,160 ethnically-matched healthy controls were included in the study. The single nucleotide polymorphism (SNP) rs374039502, which colocalizes with the genetic variant previously implicated in autoimmunity, was genotyped using a custom TaqMan assay. First, association analysis was conducted in each independent cohort using X2 test in Plink (v1.9). Subsequently, different case/control sets were meta-analyzed by the inverse variance method. Results No statistically significant differences were found when allele distributions were compared between cases and controls for any of the analyzed cohorts. Similarly, combined analysis of the different sets evidenced a lack of association of the rs374039502 variant with GCA (P = 0.421; OR (95% CI) = 0.92 (0.75-1.13)) and SSc (P = 0.500; OR (95% CI) = 1.05 (0.91-1.22)). The stratified analysis considering the main clinical subphenotypes of these diseases yielded similar negative results. Conclusion Our data suggest that the TNFSF13B functional variant does not contribute to the genetic network underlying GCA and SSc. The TNFSF13B (TNF superfamily member 13b) gene encodes BAFF, a cytokine with a crucial role in the differentiation and activation of B cells. An insertion-deletion variant (GCTGT→A) of this gene, leading to increased levels of BAFF, has been recently implicated in the genetic predisposition to several autoimmune diseases, including multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis. Based on the elevated levels of this cytokine found in patients with giant cell arteritis (GCA) and systemic sclerosis (SSc), we aimed to assess whether this functional variant also represents a novel genetic risk factor for these two disorders. A total of 1,728 biopsy-proven GCA patients from 4 European cohorts, 4,584 SSc patients from 3 European cohorts and 5,160 ethnically-matched healthy controls were included in the study. The single nucleotide polymorphism (SNP) rs374039502, which colocalizes with the genetic variant previously implicated in autoimmunity, was genotyped using a custom TaqMan assay. First, association analysis was conducted in each independent cohort using χ2 test in Plink (v1.9). Subsequently, different case/control sets were meta-analyzed by the inverse variance method. No statistically significant differences were found when allele distributions were compared between cases and controls for any of the analyzed cohorts. Similarly, combined analysis of the different sets evidenced a lack of association of the rs374039502 variant with GCA (P = 0.421; OR (95% CI) = 0.92 (0.75-1.13)) and SSc (P = 0.500; OR (95% CI) = 1.05 (0.91-1.22)). The stratified analysis considering the main clinical subphenotypes of these diseases yielded similar negative results. Our data suggest that the TNFSF13B functional variant does not contribute to the genetic network underlying GCA and SSc. Background The TNFSF13B (TNF superfamily member 13b) gene encodes BAFF, a cytokine with a crucial role in the differentiation and activation of B cells. An insertion-deletion variant (GCTGT→A) of this gene, leading to increased levels of BAFF, has been recently implicated in the genetic predisposition to several autoimmune diseases, including multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis. Based on the elevated levels of this cytokine found in patients with giant cell arteritis (GCA) and systemic sclerosis (SSc), we aimed to assess whether this functional variant also represents a novel genetic risk factor for these two disorders. Methods A total of 1,728 biopsy-proven GCA patients from 4 European cohorts, 4,584 SSc patients from 3 European cohorts and 5,160 ethnically-matched healthy controls were included in the study. The single nucleotide polymorphism (SNP) rs374039502, which colocalizes with the genetic variant previously implicated in autoimmunity, was genotyped using a custom TaqMan assay. First, association analysis was conducted in each independent cohort using χ2 test in Plink (v1.9). Subsequently, different case/control sets were meta-analyzed by the inverse variance method. Results No statistically significant differences were found when allele distributions were compared between cases and controls for any of the analyzed cohorts. Similarly, combined analysis of the different sets evidenced a lack of association of the rs374039502 variant with GCA (P = 0.421; OR (95% CI) = 0.92 (0.75–1.13)) and SSc (P = 0.500; OR (95% CI) = 1.05 (0.91–1.22)). The stratified analysis considering the main clinical subphenotypes of these diseases yielded similar negative results. Conclusion Our data suggest that the TNFSF13B functional variant does not contribute to the genetic network underlying GCA and SSc. |
| Audience | Academic |
| Author | Fonseca, Carmen Tolosa, Carlos González-Serna, David Márquez, Ana Narváez, Javier Ortego-Centeno, Norberto Martín, Javier Castañeda, Santos Cimmino, Marco A Denton, Christopher P Neumann, Thomas González-Gay, Miguel A Vaglio, Augusto Morgan, Ann W Beretta, Lorenzo Boiardi, Luigi Martinez-Valle, Ferran Carmona, Elio G Witte, Torsten Holle, Julia Simeón, Carmen P Hernández-Rodríguez, José Emmi, Giacomo Solans, Roser Salvarani, Carlo Cid, María C Herrick, Ariane L |
| AuthorAffiliation | 2 Systemic Autoimmune Diseases Unit, Hospital Clínico San Cecilio, Granada, Spain 9 Klinik für Innere Medizin III, University-Hospital Jena, Jena, Germany 18 Centre for Rheumatology, Royal Free and University College Medical School, London, UK 5 Department of Internal Medicine, Hospital Parc Tauli, Sabadell, Spain 6 Department of Rheumatology, Hospital de la Princesa, IIS-Princesa, Madrid, Spain 14 Research Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genova, Genova, Italy 16 Nephrology and Dialysis Unit, Meyer Children's University Hospital, Firenze, Italy 19 Azienda USL-IRCCS di Reggio Emilia and Università di Modena e Reggio Emilia, Reggio Emilia, Italy 4 Vasculitis Research Unit, Department of Autoimmune Diseases, Hospital Clínic, University of Barcelona, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain 17 Centre for Musculoskeletal Research and NIHR Manchester Musculoskeletal Biomedical Researc |
| AuthorAffiliation_xml | – name: 8 Hannover Medical School, Hannover, Germany – name: 13 Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy – name: 7 Department of Rheumatology, Hospital Universitari de Bellvitge, Barcelona, Spain – name: 22 Systemic Autoimmune Disease Unit, Hospital Clínico San Cecilio, Instituto de Investigación Biosanitaria de Granada (ibs.GRANADA), Granada, Spain – name: 3 Autoimmune Systemic Diseases Unit, Department of Internal Medicine, Hospital Vall d’Hebron, Autonomous University of Barcelona, Barcelona, Spain – name: 19 Azienda USL-IRCCS di Reggio Emilia and Università di Modena e Reggio Emilia, Reggio Emilia, Italy – name: 17 Centre for Musculoskeletal Research and NIHR Manchester Musculoskeletal Biomedical Research Unit, The University of Manchester, Salford Royal NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK – name: 9 Klinik für Innere Medizin III, University-Hospital Jena, Jena, Germany – name: 10 Vasculitis Clinic, Klinikum Bad Bramstedt & University Hospital of Schleswig Holstein, Bad Bramstedt, Germany – name: 15 Department of Biomedical Experimental and Clinical Sciences "Mario Serio", University of Firenze, Firenze, Italy – name: 1 Instituto de Parasitología y Biomedicina "López-Neyra", CSIC, PTS Granada, Granada, Spain – name: 4 Vasculitis Research Unit, Department of Autoimmune Diseases, Hospital Clínic, University of Barcelona, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain – name: 6 Department of Rheumatology, Hospital de la Princesa, IIS-Princesa, Madrid, Spain – name: 11 Referral Center for Systemic Autoimmune Diseases, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico di Milano, Milan, Italy – name: 2 Systemic Autoimmune Diseases Unit, Hospital Clínico San Cecilio, Granada, Spain – name: 12 Rheumatology Unit, Department of Internal Medicine, Azienda Ospedaliera Arcispedale Santa Maria Nuova, Istituto di Ricovero e Cura a Carattere Scientifico, Reggio Emilia, Italy – name: 14 Research Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genova, Genova, Italy – name: 18 Centre for Rheumatology, Royal Free and University College Medical School, London, UK – name: 21 Department of Rheumatology, Hospital Universitario Marqués de Valdecilla, IDIVAL, University of Cantabria, Santander, Spain – name: 5 Department of Internal Medicine, Hospital Parc Tauli, Sabadell, Spain – name: Peking University First Hospital, CHINA – name: 20 School of Medicine, University of Leeds and NIHR-Leeds Musculoskeletal Biomedical Research Unit, Leeds Teaching Hospitals NHS Trust, Leeds, United Kingdom – name: 16 Nephrology and Dialysis Unit, Meyer Children's University Hospital, Firenze, Italy |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30586461$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_3389_fmed_2020_587773 crossref_primary_10_1038_s41598_021_91055_z crossref_primary_10_2147_BTT_S452792 crossref_primary_10_14412_2074_2711_2020_1_22_26 |
| Cites_doi | 10.1002/art.21526 10.1586/1744666X.2016.1089173 10.1186/gm305 10.1016/j.jaut.2015.07.005 10.1002/art.38625 10.1056/NEJMoa1610528 10.1093/rheumatology/keu526 10.1186/ar4352 10.1002/art.1780330802 10.1016/j.autrev.2017.10.015 10.1002/art.1780230510 10.1136/annrheumdis-2015-207392 10.1146/annurev.immunol.21.120601.141152 |
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| Contributor | Universitat de Barcelona |
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| Copyright | COPYRIGHT 2018 Public Library of Science 2018 González-Serna et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. cc-by (c) González Serna, David et al., 2018 info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/3.0/es 2018 González-Serna et al 2018 González-Serna et al |
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| DOI | 10.1371/journal.pone.0209343 |
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| DocumentTitleAlternate | TNFSF13B variant in systemic sclerosis and giant cell arteritis |
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| Editor | Zhou, Xu-jie |
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| Notes | Competing Interests: The authors declare that they have no competing interests. Membership of the European GCA Consortium and the European Scleroderma Group can be found in the Acknowledgments. |
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| References | M Steri (ref2) 2017; 376 GG Hunder (ref10) 1990; 33 C Richard-Miceli (ref1) 2012; 4 KS van der Geest (ref4) 2014; 66 Z Brkic (ref7) 2016; 75 (ref11) 1980; 23 A Forestier (ref6) 2018; 17 F Mackay (ref3) 2003; 21 FD Carmona (ref12) 2016; 12 A Francois (ref9) 2013; 15 T Matsushita (ref8) 2006; 54 KS van der Geest (ref5) 2015; 54 L Bossini-Castillo (ref13) 2015; 64 |
| References_xml | – volume: 54 start-page: 192 issue: 1 year: 2006 ident: ref8 article-title: Elevated serum BAFF levels in patients with systemic sclerosis: enhanced BAFF signaling in systemic sclerosis B lymphocytes publication-title: Arthritis Rheum doi: 10.1002/art.21526 contributor: fullname: T Matsushita – volume: 12 start-page: 57 issue: 1 year: 2016 ident: ref12 article-title: New insights into the pathogenesis of giant cell arteritis and hopes for the clinic publication-title: Expert Rev Clin Immunol doi: 10.1586/1744666X.2016.1089173 contributor: fullname: FD Carmona – volume: 4 start-page: 6 issue: 1 year: 2012 ident: ref1 article-title: Emerging patterns of genetic overlap across autoimmune disorders publication-title: Genome Med doi: 10.1186/gm305 contributor: fullname: C Richard-Miceli – volume: 64 start-page: 53 year: 2015 ident: ref13 article-title: Immunogenetics of systemic sclerosis: Defining heritability, functional variants and shared-autoimmunity pathways publication-title: J Autoimmun doi: 10.1016/j.jaut.2015.07.005 contributor: fullname: L Bossini-Castillo – volume: 66 start-page: 1927 issue: 7 year: 2014 ident: ref4 article-title: Disturbed B cell homeostasis in newly diagnosed giant cell arteritis and polymyalgia rheumatica publication-title: Arthritis Rheumatol doi: 10.1002/art.38625 contributor: fullname: KS van der Geest – volume: 376 start-page: 1615 issue: 17 year: 2017 ident: ref2 article-title: Overexpression of the Cytokine BAFF and Autoimmunity Risk publication-title: N Engl J Med doi: 10.1056/NEJMoa1610528 contributor: fullname: M Steri – volume: 54 start-page: 1397 issue: 8 year: 2015 ident: ref5 article-title: Serum markers associated with disease activity in giant cell arteritis and polymyalgia rheumatica publication-title: Rheumatology (Oxford) doi: 10.1093/rheumatology/keu526 contributor: fullname: KS van der Geest – volume: 15 start-page: R168 issue: 5 year: 2013 ident: ref9 article-title: B lymphocytes and B-cell activating factor promote collagen and profibrotic markers expression by dermal fibroblasts in systemic sclerosis publication-title: Arthritis Res Ther doi: 10.1186/ar4352 contributor: fullname: A Francois – volume: 33 start-page: 1065 issue: 8 year: 1990 ident: ref10 article-title: The American College of Rheumatology 1990 criteria for the classification of vasculitis publication-title: Introduction. Arthritis Rheum doi: 10.1002/art.1780330802 contributor: fullname: GG Hunder – volume: 17 start-page: 244 issue: 3 year: 2018 ident: ref6 article-title: Altered B lymphocyte homeostasis and functions in systemic sclerosis publication-title: Autoimmun Rev doi: 10.1016/j.autrev.2017.10.015 contributor: fullname: A Forestier – volume: 23 start-page: 581 issue: 5 year: 1980 ident: ref11 article-title: Preliminary criteria for the classification of systemic sclerosis (scleroderma). Subcommittee for scleroderma criteria of the American Rheumatism Association Diagnostic and Therapeutic Criteria Committee publication-title: Arthritis Rheum doi: 10.1002/art.1780230510 – volume: 75 start-page: 1567 issue: 8 year: 2016 ident: ref7 article-title: The interferon type I signature is present in systemic sclerosis before overt fibrosis and might contribute to its pathogenesis through high BAFF gene expression and high collagen synthesis publication-title: Ann Rheum Dis doi: 10.1136/annrheumdis-2015-207392 contributor: fullname: Z Brkic – volume: 21 start-page: 231 year: 2003 ident: ref3 article-title: BAFF AND APRIL: a tutorial on B cell survival publication-title: Annu Rev Immunol doi: 10.1146/annurev.immunol.21.120601.141152 contributor: fullname: F Mackay |
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| Snippet | The TNFSF13B (TNF superfamily member 13b) gene encodes BAFF, a cytokine with a crucial role in the differentiation and activation of B cells. An... Background The TNFSF13B (TNF superfamily member 13b) gene encodes BAFF, a cytokine with a crucial role in the differentiation and activation of B cells. An... BACKGROUND: The TNFSF13B (TNF superfamily member 13b) gene encodes BAFF, a cytokine with a crucial role in the differentiation and activation of B cells. An... BackgroundThe TNFSF13B (TNF superfamily member 13b) gene encodes BAFF, a cytokine with a crucial role in the differentiation and activation of B cells. An... Background The TNFSF13B (TNF superfamily member 13b) gene encodes BAFF, a cytokine with a crucial role in the differentiation and activation of B cells. An... |
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| SubjectTerms | Adult Aged Aged, 80 and over Arteritis Arthritis Association analysis Autoimmune diseases B cells B-Cell Activating Factor - genetics Binding sites Biology and Life Sciences Biomedical research Biopsy BLyS protein Case-Control Studies Cell activation Chronic conditions Clonal deletion Cohort Studies Consortia Cytokines Cèl·lules B Europe Female Gene deletion Gene expression Gene polymorphism Gene Regulatory Networks - genetics Genetic aspects Genetic diversity Genetic Predisposition to Disease Genetic variance Genetic variation Genotyping Techniques Genètica molecular Giant Cell Arteritis - genetics Giant Cell Arteritis - pathology Health aspects Homeostasis Hospitals Humans INDEL Mutation Insertion Internal medicine Lymphocytes B Male Medicine Medicine and Health Sciences Middle Aged Molecular genetics Multiple sclerosis Pathogenesis Patients Physical Sciences Polymorphism Polymorphism, Single Nucleotide Research and Analysis Methods Rheumatoid arthritis Rheumatology Risk analysis Risk factors Scleroderma Scleroderma (Disease) Scleroderma, Systemic - genetics Scleroderma, Systemic - pathology Single-nucleotide polymorphism Statistical analysis Systemic diseases Systemic lupus erythematosus Systemic sclerosis Temporal arteritis Tumor necrosis factor-TNF Vein & artery diseases |
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| Title | A TNFSF13B functional variant is not involved in systemic sclerosis and giant cell arteritis susceptibility |
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