Interactions between TNFAIP3, PTPN22, and TRAF1-C5 gene polymorphisms in patients with primary Sjögren's syndrome
The aim of our study was to investigate whether TNFAIP3, PTPN22, and TRAF1-5 single nucleotide polymorphisms (SNPs) are associated with susceptibility, severity, or serological markers in primary Sjögren's syndrome (pSS). The cases and controls study was conducted between December 2021 and June...
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| Veröffentlicht in: | Archives of Rheumatology 2024-03, Vol.39 (1), p.60-70 |
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| creator | Cadena-Sandoval, Daniel Montúfar-Robles, Isela Barbosa-Cobos, Rosa Elda Hernández-Molina, Gabriela Karen Salas-García, Ana Sánchez-Zauco, Norma Ramírez-Bello, Julian |
| description | The aim of our study was to investigate whether TNFAIP3, PTPN22, and TRAF1-5 single nucleotide polymorphisms (SNPs) are associated with susceptibility, severity, or serological markers in primary Sjögren's syndrome (pSS).
The cases and controls study was conducted between December 2021 and June 2022. TNFAIP3 rs10499194C/T, rs6920220G/A, and rs2230926T/G, PTPN22 rs2476601C/T and rs33996649G/A, and TRAF1-C5 rs10818488G/A polymorphisms were genotyped in 154 female pSS patients (mean age: 45.2±6.8 years) and 313 female control subjects (mean age: 50.3±7.5 years) using the TaqMan® SNP genotyping assay. An association analysis between TNFAIP3, PTPN22, and TRAF1-C5 SNPs and susceptibility, clinical characteristics, and serological markers of pSS was performed. Interactions between TNFAIP3, PTPN22, and TRAF1-C5 SNPs were also evaluated in patients and controls.
The genotype and allele frequencies showed no association with susceptibility, severity, or serological markers of pSS. Nevertheless, several interactions between TNFAIP3 and TRAF1-C5 or TNFAIP3, PTPN22, and TRAF1-C5 genotypes were associated with susceptibility to pSS (p |
| doi_str_mv | 10.46497/ArchRheumatol.2024.10108 |
| format | Article |
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The cases and controls study was conducted between December 2021 and June 2022. TNFAIP3 rs10499194C/T, rs6920220G/A, and rs2230926T/G, PTPN22 rs2476601C/T and rs33996649G/A, and TRAF1-C5 rs10818488G/A polymorphisms were genotyped in 154 female pSS patients (mean age: 45.2±6.8 years) and 313 female control subjects (mean age: 50.3±7.5 years) using the TaqMan® SNP genotyping assay. An association analysis between TNFAIP3, PTPN22, and TRAF1-C5 SNPs and susceptibility, clinical characteristics, and serological markers of pSS was performed. Interactions between TNFAIP3, PTPN22, and TRAF1-C5 SNPs were also evaluated in patients and controls.
The genotype and allele frequencies showed no association with susceptibility, severity, or serological markers of pSS. Nevertheless, several interactions between TNFAIP3 and TRAF1-C5 or TNFAIP3, PTPN22, and TRAF1-C5 genotypes were associated with susceptibility to pSS (p<0.01).
Individual TNFAIP3, PTPN22, and TRAF1-C5 SNPs are not associated with susceptibility, severity, or serological markers of pSS. However, genetic interactions between TRAF1-C5 and TNFAIP3 or TNFAIP3, PTPN22, and TRAF1-C5 SNPs are risk factors for pSS.</description><identifier>ISSN: 2618-6500</identifier><identifier>ISSN: 2148-5046</identifier><identifier>ISSN: 1309-0291</identifier><identifier>EISSN: 2618-6500</identifier><identifier>EISSN: 1309-0283</identifier><identifier>DOI: 10.46497/ArchRheumatol.2024.10108</identifier><identifier>PMID: 38774701</identifier><language>eng</language><publisher>Turkey: Turkish League Against Rheumatism</publisher><subject>Analysis ; Antibodies ; Arthritis ; Autoimmune diseases ; Care and treatment ; Chromosomes ; Deoxyribonucleic acid ; DNA ; Exocrine glands ; Females ; Genes ; Genetic aspects ; Genetic testing ; Genomes ; Genotype & phenotype ; Haplotypes ; Health risk assessment ; Kinases ; Original ; Proteins ; Raynaud disease ; Rheumatology ; Risk factors ; Serology ; Single nucleotide polymorphisms ; Software ; Tumor necrosis factor-TNF ; Type 2 diabetes</subject><ispartof>Archives of Rheumatology, 2024-03, Vol.39 (1), p.60-70</ispartof><rights>Copyright © 2024, Turkish League Against Rheumatism.</rights><rights>COPYRIGHT 2024 Turkish League Against Rheumatism</rights><rights>Copyright Prof Sebnem Ataman, President Turkish League Against Rheumatism 2024</rights><rights>Copyright © 2024, Turkish League Against Rheumatism 2024 Turkish League Against Rheumatism</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c494t-ad37de446ece093d58f1c93645114d8b8da824db158c6e8587924bec680b6ab33</cites><orcidid>0000-0002-4153-9315 ; 0000-0003-2191-7427 ; 0000-0002-1141-452X ; 0000-0001-8415-8080 ; 0000-0002-6564-7898 ; 0000-0001-8375-1499 ; 0000-0001-7958-0391</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11104759/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11104759/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38774701$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cadena-Sandoval, Daniel</creatorcontrib><creatorcontrib>Montúfar-Robles, Isela</creatorcontrib><creatorcontrib>Barbosa-Cobos, Rosa Elda</creatorcontrib><creatorcontrib>Hernández-Molina, Gabriela</creatorcontrib><creatorcontrib>Karen Salas-García, Ana</creatorcontrib><creatorcontrib>Sánchez-Zauco, Norma</creatorcontrib><creatorcontrib>Ramírez-Bello, Julian</creatorcontrib><title>Interactions between TNFAIP3, PTPN22, and TRAF1-C5 gene polymorphisms in patients with primary Sjögren's syndrome</title><title>Archives of Rheumatology</title><addtitle>Arch Rheumatol</addtitle><description>The aim of our study was to investigate whether TNFAIP3, PTPN22, and TRAF1-5 single nucleotide polymorphisms (SNPs) are associated with susceptibility, severity, or serological markers in primary Sjögren's syndrome (pSS).
The cases and controls study was conducted between December 2021 and June 2022. TNFAIP3 rs10499194C/T, rs6920220G/A, and rs2230926T/G, PTPN22 rs2476601C/T and rs33996649G/A, and TRAF1-C5 rs10818488G/A polymorphisms were genotyped in 154 female pSS patients (mean age: 45.2±6.8 years) and 313 female control subjects (mean age: 50.3±7.5 years) using the TaqMan® SNP genotyping assay. An association analysis between TNFAIP3, PTPN22, and TRAF1-C5 SNPs and susceptibility, clinical characteristics, and serological markers of pSS was performed. Interactions between TNFAIP3, PTPN22, and TRAF1-C5 SNPs were also evaluated in patients and controls.
The genotype and allele frequencies showed no association with susceptibility, severity, or serological markers of pSS. Nevertheless, several interactions between TNFAIP3 and TRAF1-C5 or TNFAIP3, PTPN22, and TRAF1-C5 genotypes were associated with susceptibility to pSS (p<0.01).
Individual TNFAIP3, PTPN22, and TRAF1-C5 SNPs are not associated with susceptibility, severity, or serological markers of pSS. However, genetic interactions between TRAF1-C5 and TNFAIP3 or TNFAIP3, PTPN22, and TRAF1-C5 SNPs are risk factors for pSS.</description><subject>Analysis</subject><subject>Antibodies</subject><subject>Arthritis</subject><subject>Autoimmune diseases</subject><subject>Care and treatment</subject><subject>Chromosomes</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Exocrine glands</subject><subject>Females</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic testing</subject><subject>Genomes</subject><subject>Genotype & phenotype</subject><subject>Haplotypes</subject><subject>Health risk assessment</subject><subject>Kinases</subject><subject>Original</subject><subject>Proteins</subject><subject>Raynaud disease</subject><subject>Rheumatology</subject><subject>Risk factors</subject><subject>Serology</subject><subject>Single nucleotide polymorphisms</subject><subject>Software</subject><subject>Tumor necrosis factor-TNF</subject><subject>Type 2 diabetes</subject><issn>2618-6500</issn><issn>2148-5046</issn><issn>1309-0291</issn><issn>2618-6500</issn><issn>1309-0283</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptktFu0zAYhSMEYtPYKyAjJHazFDtxHOcKRRWFStOoRrm2HOdP4yqxg-0w9cX2AnsxQldGKyFf2LK_c3Rsnyh6R_CMMlrkH0un2rsWxl4G280SnNAZwQTzF9F5wgiPWYbxy6P1WXTp_RZjTGjOGE5fR2cpz3OaY3IeuaUJ4KQK2hqPKgj3AAatbxflcpVeo9V6dZsk10iaGq3vygWJ5xnagAE02G7XWze02vceaYMGGTSY4NG9Di0anO6l26Hv28eHjQNz5ZHfmdrZHt5ErxrZebg8zBfRj8Xn9fxrfPPty3Je3sSKFjTEsk7zGihloAAXaZ3xhqgiZTQjhNa84rXkCa0rknHFgGc8LxJagWIcV0xWaXoRfXryHcaqh1pN4ZzsxCGZsFKL0xOjW7GxvwQhBNM8KyaH9wcHZ3-O4IPY2tGZKbRICkonLMf8H7WRHQhtGju5qV57JcqcM05SzshEzf5DTaOGXitroNHT_ongw5GgBdmF1ttu3P_UKVg8gcpZ7x00z1ckWOwrI04qI_5URuwrM2nfHr_Rs_JvQdLfpy2_Sg</recordid><startdate>20240301</startdate><enddate>20240301</enddate><creator>Cadena-Sandoval, Daniel</creator><creator>Montúfar-Robles, Isela</creator><creator>Barbosa-Cobos, Rosa Elda</creator><creator>Hernández-Molina, Gabriela</creator><creator>Karen Salas-García, Ana</creator><creator>Sánchez-Zauco, Norma</creator><creator>Ramírez-Bello, Julian</creator><general>Turkish League Against Rheumatism</general><general>Prof Sebnem Ataman, President Turkish League Against Rheumatism</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>EDSIH</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-4153-9315</orcidid><orcidid>https://orcid.org/0000-0003-2191-7427</orcidid><orcidid>https://orcid.org/0000-0002-1141-452X</orcidid><orcidid>https://orcid.org/0000-0001-8415-8080</orcidid><orcidid>https://orcid.org/0000-0002-6564-7898</orcidid><orcidid>https://orcid.org/0000-0001-8375-1499</orcidid><orcidid>https://orcid.org/0000-0001-7958-0391</orcidid></search><sort><creationdate>20240301</creationdate><title>Interactions between TNFAIP3, PTPN22, and TRAF1-C5 gene polymorphisms in patients with primary Sjögren's syndrome</title><author>Cadena-Sandoval, Daniel ; Montúfar-Robles, Isela ; Barbosa-Cobos, Rosa Elda ; Hernández-Molina, Gabriela ; Karen Salas-García, Ana ; Sánchez-Zauco, Norma ; Ramírez-Bello, Julian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-ad37de446ece093d58f1c93645114d8b8da824db158c6e8587924bec680b6ab33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Analysis</topic><topic>Antibodies</topic><topic>Arthritis</topic><topic>Autoimmune diseases</topic><topic>Care and treatment</topic><topic>Chromosomes</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Exocrine glands</topic><topic>Females</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic testing</topic><topic>Genomes</topic><topic>Genotype & phenotype</topic><topic>Haplotypes</topic><topic>Health risk assessment</topic><topic>Kinases</topic><topic>Original</topic><topic>Proteins</topic><topic>Raynaud disease</topic><topic>Rheumatology</topic><topic>Risk factors</topic><topic>Serology</topic><topic>Single nucleotide polymorphisms</topic><topic>Software</topic><topic>Tumor necrosis factor-TNF</topic><topic>Type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cadena-Sandoval, Daniel</creatorcontrib><creatorcontrib>Montúfar-Robles, Isela</creatorcontrib><creatorcontrib>Barbosa-Cobos, Rosa Elda</creatorcontrib><creatorcontrib>Hernández-Molina, Gabriela</creatorcontrib><creatorcontrib>Karen Salas-García, Ana</creatorcontrib><creatorcontrib>Sánchez-Zauco, Norma</creatorcontrib><creatorcontrib>Ramírez-Bello, Julian</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Turkey Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Archives of Rheumatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cadena-Sandoval, Daniel</au><au>Montúfar-Robles, Isela</au><au>Barbosa-Cobos, Rosa Elda</au><au>Hernández-Molina, Gabriela</au><au>Karen Salas-García, Ana</au><au>Sánchez-Zauco, Norma</au><au>Ramírez-Bello, Julian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interactions between TNFAIP3, PTPN22, and TRAF1-C5 gene polymorphisms in patients with primary Sjögren's syndrome</atitle><jtitle>Archives of Rheumatology</jtitle><addtitle>Arch Rheumatol</addtitle><date>2024-03-01</date><risdate>2024</risdate><volume>39</volume><issue>1</issue><spage>60</spage><epage>70</epage><pages>60-70</pages><issn>2618-6500</issn><issn>2148-5046</issn><issn>1309-0291</issn><eissn>2618-6500</eissn><eissn>1309-0283</eissn><abstract>The aim of our study was to investigate whether TNFAIP3, PTPN22, and TRAF1-5 single nucleotide polymorphisms (SNPs) are associated with susceptibility, severity, or serological markers in primary Sjögren's syndrome (pSS).
The cases and controls study was conducted between December 2021 and June 2022. TNFAIP3 rs10499194C/T, rs6920220G/A, and rs2230926T/G, PTPN22 rs2476601C/T and rs33996649G/A, and TRAF1-C5 rs10818488G/A polymorphisms were genotyped in 154 female pSS patients (mean age: 45.2±6.8 years) and 313 female control subjects (mean age: 50.3±7.5 years) using the TaqMan® SNP genotyping assay. An association analysis between TNFAIP3, PTPN22, and TRAF1-C5 SNPs and susceptibility, clinical characteristics, and serological markers of pSS was performed. Interactions between TNFAIP3, PTPN22, and TRAF1-C5 SNPs were also evaluated in patients and controls.
The genotype and allele frequencies showed no association with susceptibility, severity, or serological markers of pSS. Nevertheless, several interactions between TNFAIP3 and TRAF1-C5 or TNFAIP3, PTPN22, and TRAF1-C5 genotypes were associated with susceptibility to pSS (p<0.01).
Individual TNFAIP3, PTPN22, and TRAF1-C5 SNPs are not associated with susceptibility, severity, or serological markers of pSS. However, genetic interactions between TRAF1-C5 and TNFAIP3 or TNFAIP3, PTPN22, and TRAF1-C5 SNPs are risk factors for pSS.</abstract><cop>Turkey</cop><pub>Turkish League Against Rheumatism</pub><pmid>38774701</pmid><doi>10.46497/ArchRheumatol.2024.10108</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-4153-9315</orcidid><orcidid>https://orcid.org/0000-0003-2191-7427</orcidid><orcidid>https://orcid.org/0000-0002-1141-452X</orcidid><orcidid>https://orcid.org/0000-0001-8415-8080</orcidid><orcidid>https://orcid.org/0000-0002-6564-7898</orcidid><orcidid>https://orcid.org/0000-0001-8375-1499</orcidid><orcidid>https://orcid.org/0000-0001-7958-0391</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Archives of Rheumatology, 2024-03, Vol.39 (1), p.60-70 |
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| language | eng |
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| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Analysis Antibodies Arthritis Autoimmune diseases Care and treatment Chromosomes Deoxyribonucleic acid DNA Exocrine glands Females Genes Genetic aspects Genetic testing Genomes Genotype & phenotype Haplotypes Health risk assessment Kinases Original Proteins Raynaud disease Rheumatology Risk factors Serology Single nucleotide polymorphisms Software Tumor necrosis factor-TNF Type 2 diabetes |
| title | Interactions between TNFAIP3, PTPN22, and TRAF1-C5 gene polymorphisms in patients with primary Sjögren's syndrome |
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