Gene copy-number variations (CNVs) of complement C4 and C4A deficiency in genetic risk and pathogenesis of juvenile dermatomyositis
ObjectiveComplement-mediated vasculopathy of muscle and skin are clinical features of juvenile dermatomyositis (JDM). We assess gene copy-number variations (CNVs) for complement C4 and its isotypes, C4A and C4B, in genetic risks and pathogenesis of JDM.MethodsThe study population included 105 patien...
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| Published in | Annals of the rheumatic diseases Vol. 75; no. 9; pp. 1599 - 1606 |
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| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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United States
Elsevier Limited
01.09.2016
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| Abstract | ObjectiveComplement-mediated vasculopathy of muscle and skin are clinical features of juvenile dermatomyositis (JDM). We assess gene copy-number variations (CNVs) for complement C4 and its isotypes, C4A and C4B, in genetic risks and pathogenesis of JDM.MethodsThe study population included 105 patients with JDM and 500 healthy European Americans. Gene copy-numbers (GCNs) for total C4, C4A, C4B and HLA-DRB1 genotypes were determined by Southern blots and qPCRs. Processed activation product C4d bound to erythrocytes (E-C4d) was measured by flow cytometry. Global gene-expression microarrays were performed in 19 patients with JDM and seven controls using PAXgene-blood RNA. Differential expression levels for selected genes were validated by qPCR.ResultsSignificantly lower GCNs and differences in distribution of GCN groups for total C4 and C4A were observed in JDM versus controls. Lower GCN of C4A in JDM remained among HLA DR3-positive subjects (p=0.015). Homozygous or heterozygous C4A-deficiency was present in 40.0% of patients with JDM compared with 18.2% of controls (OR=3.00 (1.87 to 4.79), p=8.2×10−6). Patients with JDM had higher levels of E-C4d than controls (p=0.004). In JDM, C4A-deficient subjects had higher levels of E-C4d (p=0.0003) and higher frequency of elevated levels of multiple serum muscle enzymes at diagnosis (p=0.0025). Microarray profiling of blood RNA revealed upregulation of type I interferon-stimulated genes and lower abundance of transcripts for T-cell and chemokine function genes in JDM, but this was less prominent among C4A-deficient or DR3-positive patients.ConclusionsComplement C4A deficiency appears to be an important factor for the genetic risk and pathogenesis of JDM, particularly in patients with a DR3-positive background. |
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| AbstractList | ObjectiveComplement-mediated vasculopathy of muscle and skin are clinical features of juvenile dermatomyositis (JDM). We assess gene copy-number variations (CNVs) for complement C4 and its isotypes, C4A and C4B, in genetic risks and pathogenesis of JDM.MethodsThe study population included 105 patients with JDM and 500 healthy European Americans. Gene copy-numbers (GCNs) for total C4, C4A, C4B and HLA-DRB1 genotypes were determined by Southern blots and qPCRs. Processed activation product C4d bound to erythrocytes (E-C4d) was measured by flow cytometry. Global gene-expression microarrays were performed in 19 patients with JDM and seven controls using PAXgene-blood RNA. Differential expression levels for selected genes were validated by qPCR.ResultsSignificantly lower GCNs and differences in distribution of GCN groups for total C4 and C4A were observed in JDM versus controls. Lower GCN of C4A in JDM remained among HLA DR3-positive subjects (p=0.015). Homozygous or heterozygous C4A-deficiency was present in 40.0% of patients with JDM compared with 18.2% of controls (OR=3.00 (1.87 to 4.79), p=8.210-6). Patients with JDM had higher levels of E-C4d than controls (p=0.004). In JDM, C4A-deficient subjects had higher levels of E-C4d (p=0.0003) and higher frequency of elevated levels of multiple serum muscle enzymes at diagnosis (p=0.0025). Microarray profiling of blood RNA revealed upregulation of type I interferon-stimulated genes and lower abundance of transcripts for T-cell and chemokine function genes in JDM, but this was less prominent among C4A-deficient or DR3-positive patients.ConclusionsComplement C4A deficiency appears to be an important factor for the genetic risk and pathogenesis of JDM, particularly in patients with a DR3-positive background. Complement-mediated vasculopathy of muscle and skin are clinical features of juvenile dermatomyositis (JDM). We assess gene copy-number variations (CNVs) for complement C4 and its isotypes, C4A and C4B, in genetic risks and pathogenesis of JDM. The study population included 105 patients with JDM and 500 healthy European Americans. Gene copy-numbers (GCNs) for total C4, C4A, C4B and HLA-DRB1 genotypes were determined by Southern blots and qPCRs. Processed activation product C4d bound to erythrocytes (E-C4d) was measured by flow cytometry. Global gene-expression microarrays were performed in 19 patients with JDM and seven controls using PAXgene-blood RNA. Differential expression levels for selected genes were validated by qPCR. Significantly lower GCNs and differences in distribution of GCN groups for total C4 and C4A were observed in JDM versus controls. Lower GCN of C4A in JDM remained among HLA DR3-positive subjects (p=0.015). Homozygous or heterozygous C4A-deficiency was present in 40.0% of patients with JDM compared with 18.2% of controls (OR=3.00 (1.87 to 4.79), p=8.2×10(-6)). Patients with JDM had higher levels of E-C4d than controls (p=0.004). In JDM, C4A-deficient subjects had higher levels of E-C4d (p=0.0003) and higher frequency of elevated levels of multiple serum muscle enzymes at diagnosis (p=0.0025). Microarray profiling of blood RNA revealed upregulation of type I interferon-stimulated genes and lower abundance of transcripts for T-cell and chemokine function genes in JDM, but this was less prominent among C4A-deficient or DR3-positive patients. Complement C4A deficiency appears to be an important factor for the genetic risk and pathogenesis of JDM, particularly in patients with a DR3-positive background. Complement-mediated vasculopathy of muscle and skin are clinical features of juvenile dermatomyositis (JDM). We assess gene copy-number variations (CNVs) for complement C4 and its isotypes, C4A and C4B, in genetic risks and pathogenesis of JDM.OBJECTIVEComplement-mediated vasculopathy of muscle and skin are clinical features of juvenile dermatomyositis (JDM). We assess gene copy-number variations (CNVs) for complement C4 and its isotypes, C4A and C4B, in genetic risks and pathogenesis of JDM.The study population included 105 patients with JDM and 500 healthy European Americans. Gene copy-numbers (GCNs) for total C4, C4A, C4B and HLA-DRB1 genotypes were determined by Southern blots and qPCRs. Processed activation product C4d bound to erythrocytes (E-C4d) was measured by flow cytometry. Global gene-expression microarrays were performed in 19 patients with JDM and seven controls using PAXgene-blood RNA. Differential expression levels for selected genes were validated by qPCR.METHODSThe study population included 105 patients with JDM and 500 healthy European Americans. Gene copy-numbers (GCNs) for total C4, C4A, C4B and HLA-DRB1 genotypes were determined by Southern blots and qPCRs. Processed activation product C4d bound to erythrocytes (E-C4d) was measured by flow cytometry. Global gene-expression microarrays were performed in 19 patients with JDM and seven controls using PAXgene-blood RNA. Differential expression levels for selected genes were validated by qPCR.Significantly lower GCNs and differences in distribution of GCN groups for total C4 and C4A were observed in JDM versus controls. Lower GCN of C4A in JDM remained among HLA DR3-positive subjects (p=0.015). Homozygous or heterozygous C4A-deficiency was present in 40.0% of patients with JDM compared with 18.2% of controls (OR=3.00 (1.87 to 4.79), p=8.2×10(-6)). Patients with JDM had higher levels of E-C4d than controls (p=0.004). In JDM, C4A-deficient subjects had higher levels of E-C4d (p=0.0003) and higher frequency of elevated levels of multiple serum muscle enzymes at diagnosis (p=0.0025). Microarray profiling of blood RNA revealed upregulation of type I interferon-stimulated genes and lower abundance of transcripts for T-cell and chemokine function genes in JDM, but this was less prominent among C4A-deficient or DR3-positive patients.RESULTSSignificantly lower GCNs and differences in distribution of GCN groups for total C4 and C4A were observed in JDM versus controls. Lower GCN of C4A in JDM remained among HLA DR3-positive subjects (p=0.015). Homozygous or heterozygous C4A-deficiency was present in 40.0% of patients with JDM compared with 18.2% of controls (OR=3.00 (1.87 to 4.79), p=8.2×10(-6)). Patients with JDM had higher levels of E-C4d than controls (p=0.004). In JDM, C4A-deficient subjects had higher levels of E-C4d (p=0.0003) and higher frequency of elevated levels of multiple serum muscle enzymes at diagnosis (p=0.0025). Microarray profiling of blood RNA revealed upregulation of type I interferon-stimulated genes and lower abundance of transcripts for T-cell and chemokine function genes in JDM, but this was less prominent among C4A-deficient or DR3-positive patients.Complement C4A deficiency appears to be an important factor for the genetic risk and pathogenesis of JDM, particularly in patients with a DR3-positive background.CONCLUSIONSComplement C4A deficiency appears to be an important factor for the genetic risk and pathogenesis of JDM, particularly in patients with a DR3-positive background. ObjectiveComplement-mediated vasculopathy of muscle and skin are clinical features of juvenile dermatomyositis (JDM). We assess gene copy-number variations (CNVs) for complement C4 and its isotypes, C4A and C4B, in genetic risks and pathogenesis of JDM.MethodsThe study population included 105 patients with JDM and 500 healthy European Americans. Gene copy-numbers (GCNs) for total C4, C4A, C4B and HLA-DRB1 genotypes were determined by Southern blots and qPCRs. Processed activation product C4d bound to erythrocytes (E-C4d) was measured by flow cytometry. Global gene-expression microarrays were performed in 19 patients with JDM and seven controls using PAXgene-blood RNA. Differential expression levels for selected genes were validated by qPCR.ResultsSignificantly lower GCNs and differences in distribution of GCN groups for total C4 and C4A were observed in JDM versus controls. Lower GCN of C4A in JDM remained among HLA DR3-positive subjects (p=0.015). Homozygous or heterozygous C4A-deficiency was present in 40.0% of patients with JDM compared with 18.2% of controls (OR=3.00 (1.87 to 4.79), p=8.2×10−6). Patients with JDM had higher levels of E-C4d than controls (p=0.004). In JDM, C4A-deficient subjects had higher levels of E-C4d (p=0.0003) and higher frequency of elevated levels of multiple serum muscle enzymes at diagnosis (p=0.0025). Microarray profiling of blood RNA revealed upregulation of type I interferon-stimulated genes and lower abundance of transcripts for T-cell and chemokine function genes in JDM, but this was less prominent among C4A-deficient or DR3-positive patients.ConclusionsComplement C4A deficiency appears to be an important factor for the genetic risk and pathogenesis of JDM, particularly in patients with a DR3-positive background. Objective Complement-mediated vasculopathy of muscle and skin are clinical features of juvenile dermatomyositis (JDM). We assess gene copy-number variations (CNVs) for complement C4 and its isotypes, C4A and C4B, in genetic risks and pathogenesis of JDM. Methods The study population included 105 patients with JDM and 500 healthy European Americans. Gene copy-numbers (GCNs) for total C4, C4A, C4B and HLA-DRB1 genotypes were determined by Southern blots and qPCRs. Processed activation product C4d bound to erythrocytes (E-C4d) was measured by flow cytometry. Global gene-expression microarrays were performed in 19 patients with JDM and seven controls using PAXgene-blood RNA. Differential expression levels for selected genes were validated by qPCR. Results Significantly lower GCNs and differences in distribution of GCN groups for total C4 and C4A were observed in JDM versus controls. Lower GCN of C4A in JDM remained among HLA DR3- positive subjects (p=0.015). Homozygous or heterozygous C4A -deficiency was present in 40.0% of patients with JDM compared with 18.2% of controls (OR=3.00 (1.87 to 4.79), p=8.2x10-6 ). Patients with JDM had higher levels of E-C4d than controls (p=0.004). In JDM, C4A -deficient subjects had higher levels of E-C4d (p=0.0003) and higher frequency of elevated levels of multiple serum muscle enzymes at diagnosis (p=0.0025). Microarray profiling of blood RNA revealed upregulation of type I interferon-stimulated genes and lower abundance of transcripts for T-cell and chemokine function genes in JDM, but this was less prominent among C4A -deficient or DR3 -positive patients. Conclusions Complement C4A deficiency appears to be an important factor for the genetic risk and pathogenesis of JDM, particularly in patients with a DR3- positive background. |
| Author | Yu, Chack Yung Spencer, Charles H Rider, Lisa G Abdul-Aziz, Rabheh Padyukov, Leonid White, Peter Zhou, Bi Miller, Frederick W Patwardhan, Anjali O'Hanlon, Terrance P Alhomosh, Alaaedin Lintner, Katherine E Newsom, David Jones, Karla B Wu, Yee Ling Lundström, Emeli |
| AuthorAffiliation | 2 Environmental Autoimmunity Group, Clinical Research Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, Maryland 1 The Research Institute at Nationwide Children’s Hospital and Department of Pediatrics, The Ohio State University, 700 Children’s Drive, Columbus Ohio 43205 3 Karolinska Institutet, Stockholm, Sweden |
| AuthorAffiliation_xml | – name: 1 The Research Institute at Nationwide Children’s Hospital and Department of Pediatrics, The Ohio State University, 700 Children’s Drive, Columbus Ohio 43205 – name: 3 Karolinska Institutet, Stockholm, Sweden – name: 2 Environmental Autoimmunity Group, Clinical Research Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, Maryland |
| Author_xml | – sequence: 1 givenname: Katherine E surname: Lintner fullname: Lintner, Katherine E email: chack-yung.yu@nationwidechildrens.org organization: Department of Pediatrics, The Research Institute at Nationwide Children's Hospital, The Ohio State University, Columbus, Ohio, USA – sequence: 2 givenname: Anjali surname: Patwardhan fullname: Patwardhan, Anjali email: chack-yung.yu@nationwidechildrens.org organization: Department of Pediatrics, The Research Institute at Nationwide Children's Hospital, The Ohio State University, Columbus, Ohio, USA – sequence: 3 givenname: Lisa G surname: Rider fullname: Rider, Lisa G email: chack-yung.yu@nationwidechildrens.org organization: Environmental Autoimmunity Group, Clinical Research Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, Maryland, USA – sequence: 4 givenname: Rabheh surname: Abdul-Aziz fullname: Abdul-Aziz, Rabheh email: chack-yung.yu@nationwidechildrens.org organization: Department of Pediatrics, The Research Institute at Nationwide Children's Hospital, The Ohio State University, Columbus, Ohio, USA – sequence: 5 givenname: Yee Ling surname: Wu fullname: Wu, Yee Ling email: chack-yung.yu@nationwidechildrens.org organization: Department of Pediatrics, The Research Institute at Nationwide Children's Hospital, The Ohio State University, Columbus, Ohio, USA – sequence: 6 givenname: Emeli surname: Lundström fullname: Lundström, Emeli email: chack-yung.yu@nationwidechildrens.org organization: Rheumatology Unit, Department of Medicine, Karolinska University Hospital, Stockholm, Sweden – sequence: 7 givenname: Leonid surname: Padyukov fullname: Padyukov, Leonid email: chack-yung.yu@nationwidechildrens.org organization: Rheumatology Unit, Department of Medicine, Karolinska University Hospital, Stockholm, Sweden – sequence: 8 givenname: Bi surname: Zhou fullname: Zhou, Bi email: chack-yung.yu@nationwidechildrens.org organization: Department of Pediatrics, The Research Institute at Nationwide Children's Hospital, The Ohio State University, Columbus, Ohio, USA – sequence: 9 givenname: Alaaedin surname: Alhomosh fullname: Alhomosh, Alaaedin email: chack-yung.yu@nationwidechildrens.org organization: Department of Pediatrics, The Research Institute at Nationwide Children's Hospital, The Ohio State University, Columbus, Ohio, USA – sequence: 10 givenname: David surname: Newsom fullname: Newsom, David email: chack-yung.yu@nationwidechildrens.org organization: Department of Pediatrics, The Research Institute at Nationwide Children's Hospital, The Ohio State University, Columbus, Ohio, USA – sequence: 11 givenname: Peter surname: White fullname: White, Peter email: chack-yung.yu@nationwidechildrens.org organization: Department of Pediatrics, The Research Institute at Nationwide Children's Hospital, The Ohio State University, Columbus, Ohio, USA – sequence: 12 givenname: Karla B surname: Jones fullname: Jones, Karla B email: chack-yung.yu@nationwidechildrens.org organization: Department of Pediatrics, The Research Institute at Nationwide Children's Hospital, The Ohio State University, Columbus, Ohio, USA – sequence: 13 givenname: Terrance P surname: O'Hanlon fullname: O'Hanlon, Terrance P email: chack-yung.yu@nationwidechildrens.org organization: Environmental Autoimmunity Group, Clinical Research Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, Maryland, USA – sequence: 14 givenname: Frederick W surname: Miller fullname: Miller, Frederick W email: chack-yung.yu@nationwidechildrens.org organization: Environmental Autoimmunity Group, Clinical Research Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, Maryland, USA – sequence: 15 givenname: Charles H surname: Spencer fullname: Spencer, Charles H email: chack-yung.yu@nationwidechildrens.org organization: Department of Pediatrics, The Research Institute at Nationwide Children's Hospital, The Ohio State University, Columbus, Ohio, USA – sequence: 16 givenname: Chack Yung surname: Yu fullname: Yu, Chack Yung email: chack-yung.yu@nationwidechildrens.org organization: Department of Pediatrics, The Research Institute at Nationwide Children's Hospital, The Ohio State University, Columbus, Ohio, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26493816$$D View this record in MEDLINE/PubMed http://kipublications.ki.se/Default.aspx?queryparsed=id:134218451$$DView record from Swedish Publication Index |
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| ContentType | Journal Article |
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| DOI | 10.1136/annrheumdis-2015-207762 |
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| Issue | 9 |
| Keywords | Gene Polymorphism Disease Activity Epidemiology Autoimmune Diseases Dermatomyositis |
| Language | English |
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| Snippet | ObjectiveComplement-mediated vasculopathy of muscle and skin are clinical features of juvenile dermatomyositis (JDM). We assess gene copy-number variations... Complement-mediated vasculopathy of muscle and skin are clinical features of juvenile dermatomyositis (JDM). We assess gene copy-number variations (CNVs) for... Objective Complement-mediated vasculopathy of muscle and skin are clinical features of juvenile dermatomyositis (JDM). We assess gene copy-number variations... |
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| SubjectTerms | Adolescent Antigens Biopsy Case-Control Studies Child Child, Preschool Complement C4 - deficiency Complement C4 - genetics Complement C4a - deficiency Complement C4a - genetics Complement C4b - genetics Dermatomyositis - genetics Disease DNA Copy Number Variations Female Genes Genetic Predisposition to Disease Genomes Genotype Haplotypes Health risk assessment Hereditary Complement Deficiency Diseases HLA-DRB1 Chains - genetics Humans Immunologic Deficiency Syndromes - genetics Male Pathogenesis Receptors, Tumor Necrosis Factor, Member 25 - blood Receptors, Tumor Necrosis Factor, Member 25 - genetics Risk Factors Tumor necrosis factor-TNF White people White People - genetics |
| Title | Gene copy-number variations (CNVs) of complement C4 and C4A deficiency in genetic risk and pathogenesis of juvenile dermatomyositis |
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