Involvement of functional polymorphisms in the TNFA gene in the pathogenesis of autoimmune thyroid diseases and production of anti-thyrotropin receptor antibody
The severity of Hashimoto's disease (HD) and intractability of Graves' disease (GD) varies among patients. Severity of HD is associated with the functional +874A/T polymorphism for interferon-γ, an inflammatory cytokine. To clarify the association between functional polymorphisms in two ot...
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| Veröffentlicht in: | Clinical and experimental immunology 2009-05, Vol.156 (2), p.199-204 |
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| description | The severity of Hashimoto's disease (HD) and intractability of Graves' disease (GD) varies among patients. Severity of HD is associated with the functional +874A/T polymorphism for interferon-γ, an inflammatory cytokine. To clarify the association between functional polymorphisms in two other inflammatory cytokine genes [tumour necrosis factor (TNF)-α and interleukin (IL)-2] and the severity of autoimmune thyroid disease (AITD), we examined the TNF-α-1031T/C, TNF-α-857C/T and IL-2 -330T/G polymorphisms in genomic DNA samples. We genotyped 41 patients with intractable GD, 34 patients with GD in remission, 41 patients with severe HD, 36 patients with mild HD and 70 healthy controls. The frequency of carriers of TNF-α-1031C (CT + CC), which correlates with higher TNF-α production, was significantly higher in HD and GD patients than in controls, but was not associated with the severity of HD. In GD patients, the levels of anti-thyrotropin receptor antibody (TRAb) at onset of the disease was higher in patients with the TNF-α-857T (CT + TT) genotype, which correlates with higher TNF-α production, than in those with the -857CC genotype. We found no differences in the IL-2 -330T/G polymorphism among groups of AITD patients. In conclusion, the functional -1031T/C polymorphism of the TNFA gene is associated with the development of AITD and the functional -857C/T polymorphism is associated with the levels of TRAb in active GD patients. |
| doi_str_mv | 10.1111/j.1365-2249.2009.03884.x |
| format | Article |
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Severity of HD is associated with the functional +874A/T polymorphism for interferon-γ, an inflammatory cytokine. To clarify the association between functional polymorphisms in two other inflammatory cytokine genes [tumour necrosis factor (TNF)-α and interleukin (IL)-2] and the severity of autoimmune thyroid disease (AITD), we examined the TNF-α-1031T/C, TNF-α-857C/T and IL-2 -330T/G polymorphisms in genomic DNA samples. We genotyped 41 patients with intractable GD, 34 patients with GD in remission, 41 patients with severe HD, 36 patients with mild HD and 70 healthy controls. The frequency of carriers of TNF-α-1031C (CT + CC), which correlates with higher TNF-α production, was significantly higher in HD and GD patients than in controls, but was not associated with the severity of HD. In GD patients, the levels of anti-thyrotropin receptor antibody (TRAb) at onset of the disease was higher in patients with the TNF-α-857T (CT + TT) genotype, which correlates with higher TNF-α production, than in those with the -857CC genotype. We found no differences in the IL-2 -330T/G polymorphism among groups of AITD patients. In conclusion, the functional -1031T/C polymorphism of the TNFA gene is associated with the development of AITD and the functional -857C/T polymorphism is associated with the levels of TRAb in active GD patients.</description><identifier>ISSN: 0009-9104</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1111/j.1365-2249.2009.03884.x</identifier><identifier>PMID: 19250279</identifier><identifier>CODEN: CEXIAL</identifier><language>eng</language><publisher>Oxford, UK: Oxford, UK : Blackwell Publishing Ltd</publisher><subject>Acute Disease ; Adult ; Analytical, structural and metabolic biochemistry ; Autoantibodies - blood ; Biological and medical sciences ; Case-Control Studies ; Chi-Square Distribution ; disease severity ; Endocrinopathies ; Female ; Fundamental and applied biological sciences. Psychology ; Genetic Predisposition to Disease ; Genotype ; Graves Disease - genetics ; Graves Disease - immunology ; Hashimoto Disease - genetics ; Hashimoto Disease - immunology ; Humans ; IL-2 ; Interferon-gamma - genetics ; Interleukin-2 - genetics ; Iodide Peroxidase - immunology ; Male ; Medical sciences ; Middle Aged ; Non tumoral diseases. Target tissue resistance. Benign neoplasms ; Polymorphism, Single Nucleotide ; Prognosis ; Receptors, Thyrotropin - immunology ; single nucleotide polymorphism ; Statistics, Nonparametric ; Thyroglobulin - immunology ; Thyroid. Thyroid axis (diseases) ; TNF-α ; TRAb ; Translational Studies ; Tumor Necrosis Factor-alpha - genetics</subject><ispartof>Clinical and experimental immunology, 2009-05, Vol.156 (2), p.199-204</ispartof><rights>2009 British Society for Immunology</rights><rights>2009 INIST-CNRS</rights><rights>Journal Compilation © 2009 British Society for Immunology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5574-5f0ab38fa15e2c1bea5eda01d14a2b93e2b050778f803726328924da9be083c33</citedby><cites>FETCH-LOGICAL-c5574-5f0ab38fa15e2c1bea5eda01d14a2b93e2b050778f803726328924da9be083c33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2759465/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2759465/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21336120$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19250279$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Inoue, N</creatorcontrib><creatorcontrib>Watanabe, M</creatorcontrib><creatorcontrib>Nanba, T</creatorcontrib><creatorcontrib>Wada, M</creatorcontrib><creatorcontrib>Akamizu, T</creatorcontrib><creatorcontrib>Iwatani, Y</creatorcontrib><title>Involvement of functional polymorphisms in the TNFA gene in the pathogenesis of autoimmune thyroid diseases and production of anti-thyrotropin receptor antibody</title><title>Clinical and experimental immunology</title><addtitle>Clin Exp Immunol</addtitle><description>The severity of Hashimoto's disease (HD) and intractability of Graves' disease (GD) varies among patients. Severity of HD is associated with the functional +874A/T polymorphism for interferon-γ, an inflammatory cytokine. To clarify the association between functional polymorphisms in two other inflammatory cytokine genes [tumour necrosis factor (TNF)-α and interleukin (IL)-2] and the severity of autoimmune thyroid disease (AITD), we examined the TNF-α-1031T/C, TNF-α-857C/T and IL-2 -330T/G polymorphisms in genomic DNA samples. We genotyped 41 patients with intractable GD, 34 patients with GD in remission, 41 patients with severe HD, 36 patients with mild HD and 70 healthy controls. The frequency of carriers of TNF-α-1031C (CT + CC), which correlates with higher TNF-α production, was significantly higher in HD and GD patients than in controls, but was not associated with the severity of HD. In GD patients, the levels of anti-thyrotropin receptor antibody (TRAb) at onset of the disease was higher in patients with the TNF-α-857T (CT + TT) genotype, which correlates with higher TNF-α production, than in those with the -857CC genotype. We found no differences in the IL-2 -330T/G polymorphism among groups of AITD patients. In conclusion, the functional -1031T/C polymorphism of the TNFA gene is associated with the development of AITD and the functional -857C/T polymorphism is associated with the levels of TRAb in active GD patients.</description><subject>Acute Disease</subject><subject>Adult</subject><subject>Analytical, structural and metabolic biochemistry</subject><subject>Autoantibodies - blood</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Chi-Square Distribution</subject><subject>disease severity</subject><subject>Endocrinopathies</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Graves Disease - genetics</subject><subject>Graves Disease - immunology</subject><subject>Hashimoto Disease - genetics</subject><subject>Hashimoto Disease - immunology</subject><subject>Humans</subject><subject>IL-2</subject><subject>Interferon-gamma - genetics</subject><subject>Interleukin-2 - genetics</subject><subject>Iodide Peroxidase - immunology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Non tumoral diseases. Target tissue resistance. Benign neoplasms</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Prognosis</subject><subject>Receptors, Thyrotropin - immunology</subject><subject>single nucleotide polymorphism</subject><subject>Statistics, Nonparametric</subject><subject>Thyroglobulin - immunology</subject><subject>Thyroid. Thyroid axis (diseases)</subject><subject>TNF-α</subject><subject>TRAb</subject><subject>Translational Studies</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><issn>0009-9104</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNks2O0zAQxyMEYsvCK4AvcEvxRxInB5BW1S5UWsGB3bM1SSatq8QOdtLdvg2PipOWAifwxfbMb_4z9kwUEUaXLKz3uyUTWRpznhRLTmmxpCLPk-Xjk2hxdjyNFjS44oLR5CJ64f0uXLMs48-jC1bwlHJZLKIfa7O37R47NAOxDWlGUw3aGmhJb9tDZ12_1b7zRBsybJHcfbm5Ihs0-MvQw7C1k8FrPwnAOFjddWMghu3BWV2TWnsEj56AqUnvbD3OKWbaDDqeucHZPkg6rLAfrJs9pa0PL6NnDbQeX532y-j-5vpu9Tm-_fppvbq6jas0lUmcNhRKkTfAUuQVKxFSrIGymiXAy0IgL2lKpcybnArJM8Hzgic1FCXSXFRCXEYfj7r9WHZYV-E_HLSqd7oDd1AWtPrbY_RWbexecZkWSZYGgXcnAWe_j-gH1WlfYduCQTt6lUk2_fm_QU5lwqTkAcyPYOWs9w6bczWMqmkO1E5N7VZTu9U0B2qeA_UYQl__-ZrfgafGB-DtCQBfQds4MJX2Z44zITLGaeA-HLkH3eLhvwtQq-v1dArxb47xDVgFGxdy3H_jlAnKMpZxIcVPvqjcww</recordid><startdate>200905</startdate><enddate>200905</enddate><creator>Inoue, N</creator><creator>Watanabe, M</creator><creator>Nanba, T</creator><creator>Wada, M</creator><creator>Akamizu, T</creator><creator>Iwatani, Y</creator><general>Oxford, UK : Blackwell Publishing Ltd</general><general>Blackwell Publishing Ltd</general><general>Blackwell</general><general>Blackwell Science Inc</general><scope>FBQ</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200905</creationdate><title>Involvement of functional polymorphisms in the TNFA gene in the pathogenesis of autoimmune thyroid diseases and production of anti-thyrotropin receptor antibody</title><author>Inoue, N ; Watanabe, M ; Nanba, T ; Wada, M ; Akamizu, T ; Iwatani, Y</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5574-5f0ab38fa15e2c1bea5eda01d14a2b93e2b050778f803726328924da9be083c33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Acute Disease</topic><topic>Adult</topic><topic>Analytical, structural and metabolic biochemistry</topic><topic>Autoantibodies - blood</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>Chi-Square Distribution</topic><topic>disease severity</topic><topic>Endocrinopathies</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Graves Disease - genetics</topic><topic>Graves Disease - immunology</topic><topic>Hashimoto Disease - genetics</topic><topic>Hashimoto Disease - immunology</topic><topic>Humans</topic><topic>IL-2</topic><topic>Interferon-gamma - genetics</topic><topic>Interleukin-2 - genetics</topic><topic>Iodide Peroxidase - immunology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Non tumoral diseases. Target tissue resistance. Benign neoplasms</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Prognosis</topic><topic>Receptors, Thyrotropin - immunology</topic><topic>single nucleotide polymorphism</topic><topic>Statistics, Nonparametric</topic><topic>Thyroglobulin - immunology</topic><topic>Thyroid. Thyroid axis (diseases)</topic><topic>TNF-α</topic><topic>TRAb</topic><topic>Translational Studies</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Inoue, N</creatorcontrib><creatorcontrib>Watanabe, M</creatorcontrib><creatorcontrib>Nanba, T</creatorcontrib><creatorcontrib>Wada, M</creatorcontrib><creatorcontrib>Akamizu, T</creatorcontrib><creatorcontrib>Iwatani, Y</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical and experimental immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Inoue, N</au><au>Watanabe, M</au><au>Nanba, T</au><au>Wada, M</au><au>Akamizu, T</au><au>Iwatani, Y</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of functional polymorphisms in the TNFA gene in the pathogenesis of autoimmune thyroid diseases and production of anti-thyrotropin receptor antibody</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>2009-05</date><risdate>2009</risdate><volume>156</volume><issue>2</issue><spage>199</spage><epage>204</epage><pages>199-204</pages><issn>0009-9104</issn><eissn>1365-2249</eissn><coden>CEXIAL</coden><abstract>The severity of Hashimoto's disease (HD) and intractability of Graves' disease (GD) varies among patients. Severity of HD is associated with the functional +874A/T polymorphism for interferon-γ, an inflammatory cytokine. To clarify the association between functional polymorphisms in two other inflammatory cytokine genes [tumour necrosis factor (TNF)-α and interleukin (IL)-2] and the severity of autoimmune thyroid disease (AITD), we examined the TNF-α-1031T/C, TNF-α-857C/T and IL-2 -330T/G polymorphisms in genomic DNA samples. We genotyped 41 patients with intractable GD, 34 patients with GD in remission, 41 patients with severe HD, 36 patients with mild HD and 70 healthy controls. The frequency of carriers of TNF-α-1031C (CT + CC), which correlates with higher TNF-α production, was significantly higher in HD and GD patients than in controls, but was not associated with the severity of HD. In GD patients, the levels of anti-thyrotropin receptor antibody (TRAb) at onset of the disease was higher in patients with the TNF-α-857T (CT + TT) genotype, which correlates with higher TNF-α production, than in those with the -857CC genotype. We found no differences in the IL-2 -330T/G polymorphism among groups of AITD patients. In conclusion, the functional -1031T/C polymorphism of the TNFA gene is associated with the development of AITD and the functional -857C/T polymorphism is associated with the levels of TRAb in active GD patients.</abstract><cop>Oxford, UK</cop><pub>Oxford, UK : Blackwell Publishing Ltd</pub><pmid>19250279</pmid><doi>10.1111/j.1365-2249.2009.03884.x</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Oxford University Press Journals All Titles (1996-Current); PubMed Central; Alma/SFX Local Collection |
| subjects | Acute Disease Adult Analytical, structural and metabolic biochemistry Autoantibodies - blood Biological and medical sciences Case-Control Studies Chi-Square Distribution disease severity Endocrinopathies Female Fundamental and applied biological sciences. Psychology Genetic Predisposition to Disease Genotype Graves Disease - genetics Graves Disease - immunology Hashimoto Disease - genetics Hashimoto Disease - immunology Humans IL-2 Interferon-gamma - genetics Interleukin-2 - genetics Iodide Peroxidase - immunology Male Medical sciences Middle Aged Non tumoral diseases. Target tissue resistance. Benign neoplasms Polymorphism, Single Nucleotide Prognosis Receptors, Thyrotropin - immunology single nucleotide polymorphism Statistics, Nonparametric Thyroglobulin - immunology Thyroid. Thyroid axis (diseases) TNF-α TRAb Translational Studies Tumor Necrosis Factor-alpha - genetics |
| title | Involvement of functional polymorphisms in the TNFA gene in the pathogenesis of autoimmune thyroid diseases and production of anti-thyrotropin receptor antibody |
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