Experimental autoimmune thyroiditis in nonobese diabetic mice lacking interferon regulatory factor-1
Interferon regulatory factor-1 (IRF-1) is pivotal in the regulation of interferon (IFN)-mediated immune reactions, and studies suggest that IRF-1 is involved in the development of autoimmune diseases. IRF-1+/+, +/−, and −/− nonobese diabetic (NOD) mice were immunized with mouse thyroglobulin (mTg) t...
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| Veröffentlicht in: | Clinical immunology (Orlando, Fla.) Fla.), 2004-11, Vol.113 (2), p.187-192 |
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| creator | Jin, Zhongtian Mori, Kouki Fujimori, Keisei Hoshikawa, Saeko Tani, Jun-ichi Satoh, Jo Ito, Sadayoshi Satomi, Susumu Yoshida, Katsumi |
| description | Interferon regulatory factor-1 (IRF-1) is pivotal in the regulation of interferon (IFN)-mediated immune reactions, and studies suggest that IRF-1 is involved in the development of autoimmune diseases. IRF-1+/+, +/−, and −/− nonobese diabetic (NOD) mice were immunized with mouse thyroglobulin (mTg) to determine whether IRF-1 is required in experimental autoimmune thyroiditis (EAT), a murine model for Hashimoto's thyroiditis (HT). IRF-1-deficient mice developed EAT and anti-mTg antibodies comparable to IRF-1+/+ and +/− mice. Whereas both CD4+ and CD8+ T cells were found in thyroids of IRF-1+/+ mice, the latter was not in IRF-1−/− mice. Major histocompatibility complex class II antigen was comparably expressed in thyroids of IRF-1+/+ and −/− mice. Lack of IRF-1 resulted in decreased CD8+ T cell number in the spleen and reduced IFNγ production by splenocytes. Our results suggest that IRF-1 is not pivotal in EAT in NOD mice. |
| doi_str_mv | 10.1016/j.clim.2004.06.008 |
| format | Article |
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IRF-1+/+, +/−, and −/− nonobese diabetic (NOD) mice were immunized with mouse thyroglobulin (mTg) to determine whether IRF-1 is required in experimental autoimmune thyroiditis (EAT), a murine model for Hashimoto's thyroiditis (HT). IRF-1-deficient mice developed EAT and anti-mTg antibodies comparable to IRF-1+/+ and +/− mice. Whereas both CD4+ and CD8+ T cells were found in thyroids of IRF-1+/+ mice, the latter was not in IRF-1−/− mice. Major histocompatibility complex class II antigen was comparably expressed in thyroids of IRF-1+/+ and −/− mice. Lack of IRF-1 resulted in decreased CD8+ T cell number in the spleen and reduced IFNγ production by splenocytes. Our results suggest that IRF-1 is not pivotal in EAT in NOD mice.</description><identifier>ISSN: 1521-6616</identifier><identifier>EISSN: 1521-7035</identifier><identifier>DOI: 10.1016/j.clim.2004.06.008</identifier><identifier>PMID: 15451476</identifier><identifier>CODEN: CLIIFY</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; CD4-Positive T-Lymphocytes - immunology ; CD8-Positive T-Lymphocytes - immunology ; Cell Differentiation - immunology ; Disease Models, Animal ; DNA-Binding Proteins - deficiency ; Flow Cytometry ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Immunohistochemistry ; Immunopathology ; Interferon Regulatory Factor-1 ; IRF-1 ; Medical sciences ; Mice ; Mice, Inbred NOD ; NOD mice ; Phosphoproteins - deficiency ; Spleen - immunology ; Thyroglobulin - immunology ; Thyroid Gland - immunology ; Thyroid Gland - pathology ; Thyroiditis ; Thyroiditis, Autoimmune - immunology ; Thyroiditis, Autoimmune - pathology</subject><ispartof>Clinical immunology (Orlando, Fla.), 2004-11, Vol.113 (2), p.187-192</ispartof><rights>2004 Elsevier Inc.</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c413t-e7592d2ddcb4d7c41128cde7affa33ea22a090876c8d84d8d12883fd2ba5bd7e3</citedby><cites>FETCH-LOGICAL-c413t-e7592d2ddcb4d7c41128cde7affa33ea22a090876c8d84d8d12883fd2ba5bd7e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.clim.2004.06.008$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16173643$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15451476$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jin, Zhongtian</creatorcontrib><creatorcontrib>Mori, Kouki</creatorcontrib><creatorcontrib>Fujimori, Keisei</creatorcontrib><creatorcontrib>Hoshikawa, Saeko</creatorcontrib><creatorcontrib>Tani, Jun-ichi</creatorcontrib><creatorcontrib>Satoh, Jo</creatorcontrib><creatorcontrib>Ito, Sadayoshi</creatorcontrib><creatorcontrib>Satomi, Susumu</creatorcontrib><creatorcontrib>Yoshida, Katsumi</creatorcontrib><title>Experimental autoimmune thyroiditis in nonobese diabetic mice lacking interferon regulatory factor-1</title><title>Clinical immunology (Orlando, Fla.)</title><addtitle>Clin Immunol</addtitle><description>Interferon regulatory factor-1 (IRF-1) is pivotal in the regulation of interferon (IFN)-mediated immune reactions, and studies suggest that IRF-1 is involved in the development of autoimmune diseases. IRF-1+/+, +/−, and −/− nonobese diabetic (NOD) mice were immunized with mouse thyroglobulin (mTg) to determine whether IRF-1 is required in experimental autoimmune thyroiditis (EAT), a murine model for Hashimoto's thyroiditis (HT). IRF-1-deficient mice developed EAT and anti-mTg antibodies comparable to IRF-1+/+ and +/− mice. Whereas both CD4+ and CD8+ T cells were found in thyroids of IRF-1+/+ mice, the latter was not in IRF-1−/− mice. Major histocompatibility complex class II antigen was comparably expressed in thyroids of IRF-1+/+ and −/− mice. Lack of IRF-1 resulted in decreased CD8+ T cell number in the spleen and reduced IFNγ production by splenocytes. Our results suggest that IRF-1 is not pivotal in EAT in NOD mice.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>Cell Differentiation - immunology</subject><subject>Disease Models, Animal</subject><subject>DNA-Binding Proteins - deficiency</subject><subject>Flow Cytometry</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Immunohistochemistry</subject><subject>Immunopathology</subject><subject>Interferon Regulatory Factor-1</subject><subject>IRF-1</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred NOD</subject><subject>NOD mice</subject><subject>Phosphoproteins - deficiency</subject><subject>Spleen - immunology</subject><subject>Thyroglobulin - immunology</subject><subject>Thyroid Gland - immunology</subject><subject>Thyroid Gland - pathology</subject><subject>Thyroiditis</subject><subject>Thyroiditis, Autoimmune - immunology</subject><subject>Thyroiditis, Autoimmune - pathology</subject><issn>1521-6616</issn><issn>1521-7035</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1r3DAQhkVpaT7aP9BD0aW92dWHLWmhlxDSJrCQS3sWsjROtbWlrSSH7L-vljXklpxmmHneYXhfhD5R0lJCxbddayc_t4yQriWiJUS9Qee0Z7SRhPdv114IKs7QRc47QkjPmHiPzmjf9bST4hy5m6c9JD9DKGbCZinRz_MSAJc_hxS988Vn7AMOMcQBMmDnzQDFWzx7C3gy9q8PD5UokEZIMeAED8tkSkwHPBpba0M_oHejmTJ8XOsl-v3j5tf1bbO9_3l3fbVtbEd5aUD2G-aYc3bonKwzypR1IM04Gs7BMGbIhigprHKqc8rVveKjY4PpByeBX6Kvp7v7FP8tkIuefbYwTSZAXLIWYkN5J9irIJVSSclUBdkJtCnmnGDU-2qWSQdNiT6GoHf6GII-hqCJ0DWEKvq8Xl-GGdyzZHW9Al9WwGRrpjGZYH1-5gSVXHS8ct9PHFTTHj0kna2HYMH5BLZoF_1Lf_wHgvuntg</recordid><startdate>20041101</startdate><enddate>20041101</enddate><creator>Jin, Zhongtian</creator><creator>Mori, Kouki</creator><creator>Fujimori, Keisei</creator><creator>Hoshikawa, Saeko</creator><creator>Tani, Jun-ichi</creator><creator>Satoh, Jo</creator><creator>Ito, Sadayoshi</creator><creator>Satomi, Susumu</creator><creator>Yoshida, Katsumi</creator><general>Elsevier Inc</general><general>Elsevier</general><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>H94</scope><scope>7X8</scope></search><sort><creationdate>20041101</creationdate><title>Experimental autoimmune thyroiditis in nonobese diabetic mice lacking interferon regulatory factor-1</title><author>Jin, Zhongtian ; Mori, Kouki ; Fujimori, Keisei ; Hoshikawa, Saeko ; Tani, Jun-ichi ; Satoh, Jo ; Ito, Sadayoshi ; Satomi, Susumu ; Yoshida, Katsumi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-e7592d2ddcb4d7c41128cde7affa33ea22a090876c8d84d8d12883fd2ba5bd7e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>CD8-Positive T-Lymphocytes - immunology</topic><topic>Cell Differentiation - immunology</topic><topic>Disease Models, Animal</topic><topic>DNA-Binding Proteins - deficiency</topic><topic>Flow Cytometry</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Immunohistochemistry</topic><topic>Immunopathology</topic><topic>Interferon Regulatory Factor-1</topic><topic>IRF-1</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred NOD</topic><topic>NOD mice</topic><topic>Phosphoproteins - deficiency</topic><topic>Spleen - immunology</topic><topic>Thyroglobulin - immunology</topic><topic>Thyroid Gland - immunology</topic><topic>Thyroid Gland - pathology</topic><topic>Thyroiditis</topic><topic>Thyroiditis, Autoimmune - immunology</topic><topic>Thyroiditis, Autoimmune - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jin, Zhongtian</creatorcontrib><creatorcontrib>Mori, Kouki</creatorcontrib><creatorcontrib>Fujimori, Keisei</creatorcontrib><creatorcontrib>Hoshikawa, Saeko</creatorcontrib><creatorcontrib>Tani, Jun-ichi</creatorcontrib><creatorcontrib>Satoh, Jo</creatorcontrib><creatorcontrib>Ito, Sadayoshi</creatorcontrib><creatorcontrib>Satomi, Susumu</creatorcontrib><creatorcontrib>Yoshida, Katsumi</creatorcontrib><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>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical immunology (Orlando, Fla.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jin, Zhongtian</au><au>Mori, Kouki</au><au>Fujimori, Keisei</au><au>Hoshikawa, Saeko</au><au>Tani, Jun-ichi</au><au>Satoh, Jo</au><au>Ito, Sadayoshi</au><au>Satomi, Susumu</au><au>Yoshida, Katsumi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Experimental autoimmune thyroiditis in nonobese diabetic mice lacking interferon regulatory factor-1</atitle><jtitle>Clinical immunology (Orlando, Fla.)</jtitle><addtitle>Clin Immunol</addtitle><date>2004-11-01</date><risdate>2004</risdate><volume>113</volume><issue>2</issue><spage>187</spage><epage>192</epage><pages>187-192</pages><issn>1521-6616</issn><eissn>1521-7035</eissn><coden>CLIIFY</coden><abstract>Interferon regulatory factor-1 (IRF-1) is pivotal in the regulation of interferon (IFN)-mediated immune reactions, and studies suggest that IRF-1 is involved in the development of autoimmune diseases. IRF-1+/+, +/−, and −/− nonobese diabetic (NOD) mice were immunized with mouse thyroglobulin (mTg) to determine whether IRF-1 is required in experimental autoimmune thyroiditis (EAT), a murine model for Hashimoto's thyroiditis (HT). IRF-1-deficient mice developed EAT and anti-mTg antibodies comparable to IRF-1+/+ and +/− mice. Whereas both CD4+ and CD8+ T cells were found in thyroids of IRF-1+/+ mice, the latter was not in IRF-1−/− mice. Major histocompatibility complex class II antigen was comparably expressed in thyroids of IRF-1+/+ and −/− mice. Lack of IRF-1 resulted in decreased CD8+ T cell number in the spleen and reduced IFNγ production by splenocytes. Our results suggest that IRF-1 is not pivotal in EAT in NOD mice.</abstract><cop>San Diego, CA</cop><pub>Elsevier Inc</pub><pmid>15451476</pmid><doi>10.1016/j.clim.2004.06.008</doi><tpages>6</tpages></addata></record> |
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| subjects | Animals Biological and medical sciences CD4-Positive T-Lymphocytes - immunology CD8-Positive T-Lymphocytes - immunology Cell Differentiation - immunology Disease Models, Animal DNA-Binding Proteins - deficiency Flow Cytometry Fundamental and applied biological sciences. Psychology Fundamental immunology Immunohistochemistry Immunopathology Interferon Regulatory Factor-1 IRF-1 Medical sciences Mice Mice, Inbred NOD NOD mice Phosphoproteins - deficiency Spleen - immunology Thyroglobulin - immunology Thyroid Gland - immunology Thyroid Gland - pathology Thyroiditis Thyroiditis, Autoimmune - immunology Thyroiditis, Autoimmune - pathology |
| title | Experimental autoimmune thyroiditis in nonobese diabetic mice lacking interferon regulatory factor-1 |
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