Reduction in experimental autoimmune thyroiditis by IgG Fc fragments bearing regRF epitopes
Previously, we identified a new immunoregulatory factor, the production of which provides rats with resistance to certain experimental autoimmune diseases. It has been named regulatory rheumatoid factor (regRF). RegRF inhibits the expansion of CD4 T lymphocytes by killing activated cells. CD4 T cell...
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| Veröffentlicht in: | Immunologic research 2023-02, Vol.71 (1), p.83-91 |
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| creator | Beduleva, Liubov Sidorov, Alexandr Terentiev, Alexey Varaksin, Viktor Fomina, Kseniya Menshikov, Igor |
| description | Previously, we identified a new immunoregulatory factor, the production of which provides rats with resistance to certain experimental autoimmune diseases. It has been named regulatory rheumatoid factor (regRF). RegRF inhibits the expansion of CD4 T lymphocytes by killing activated cells. CD4 T cells are essential for antibody production against a majority of antigens and for the generation of cytotoxic T cells; therefore, regRF is an attractive therapeutic biotarget for T-cell and antibody-mediated autoimmune diseases. RegRF is anti-idiotypic antibodies that have a shared paratope in addition to an individual paratope. Epitopes specific to the shared regRF paratope (regRF epitopes) can be obtained on conformers of IgG Fc fragments. Immunization with Fc fragments carrying regRF epitopes reduces rat collagen–induced arthritis and diminishes experimental autoimmune encephalomyelitis. The aim of this study was to determine whether IgG Fc fragments bearing regRF epitopes suppress experimental autoimmune thyroiditis (EAT). Four weeks after EAT induction, rats were immunized with IgG Fc fragments exhibiting regRF epitopes. Histology studies of the thyroid were performed 4 weeks later. Thyroid function and other parameters were also evaluated. Treatment of rats with Fc fragments bearing regRF epitopes decreased the number of rats affected by EAT, significantly decreased the extent of thyroid damage, prevented thyroid metaplasia, and restored normal thyroid hormone production. Therefore, RegRF is a promising biotarget in autoimmune thyroiditis, and Fc fragments bearing regRF epitopes are a potential therapeutic agent for that condition. |
| doi_str_mv | 10.1007/s12026-022-09337-1 |
| format | Article |
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It has been named regulatory rheumatoid factor (regRF). RegRF inhibits the expansion of CD4 T lymphocytes by killing activated cells. CD4 T cells are essential for antibody production against a majority of antigens and for the generation of cytotoxic T cells; therefore, regRF is an attractive therapeutic biotarget for T-cell and antibody-mediated autoimmune diseases. RegRF is anti-idiotypic antibodies that have a shared paratope in addition to an individual paratope. Epitopes specific to the shared regRF paratope (regRF epitopes) can be obtained on conformers of IgG Fc fragments. Immunization with Fc fragments carrying regRF epitopes reduces rat collagen–induced arthritis and diminishes experimental autoimmune encephalomyelitis. The aim of this study was to determine whether IgG Fc fragments bearing regRF epitopes suppress experimental autoimmune thyroiditis (EAT). Four weeks after EAT induction, rats were immunized with IgG Fc fragments exhibiting regRF epitopes. Histology studies of the thyroid were performed 4 weeks later. Thyroid function and other parameters were also evaluated. Treatment of rats with Fc fragments bearing regRF epitopes decreased the number of rats affected by EAT, significantly decreased the extent of thyroid damage, prevented thyroid metaplasia, and restored normal thyroid hormone production. Therefore, RegRF is a promising biotarget in autoimmune thyroiditis, and Fc fragments bearing regRF epitopes are a potential therapeutic agent for that condition.</description><identifier>ISSN: 0257-277X</identifier><identifier>EISSN: 1559-0755</identifier><identifier>DOI: 10.1007/s12026-022-09337-1</identifier><identifier>PMID: 36344864</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Allergology ; Animals ; Antibodies ; Antigens ; Arthritis ; Autoimmune diseases ; Biomedical and Life Sciences ; Biomedicine ; CD4 antigen ; Chemical compounds ; Collagen ; Cytotoxicity ; Damage prevention ; Disease Models, Animal ; Epitopes ; Experimental allergic encephalomyelitis ; Experimental autoimmune thyroiditis ; Fragments ; Hashimoto Disease - immunology ; Hashimoto Disease - therapy ; Histology ; Immunization ; Immunoglobulin Fc Fragments - therapeutic use ; Immunoglobulin G ; Immunology ; Immunoregulation ; Internal Medicine ; Lymphocytes ; Lymphocytes T ; Medicine/Public Health ; Metaplasia ; Original Article ; Pharmacology ; Rats ; Rheumatoid factor ; Rheumatoid Factor - immunology ; Thyroid ; Thyroid gland ; Thyroiditis ; Thyroiditis, Autoimmune - therapy</subject><ispartof>Immunologic research, 2023-02, Vol.71 (1), p.83-91</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2022. 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It has been named regulatory rheumatoid factor (regRF). RegRF inhibits the expansion of CD4 T lymphocytes by killing activated cells. CD4 T cells are essential for antibody production against a majority of antigens and for the generation of cytotoxic T cells; therefore, regRF is an attractive therapeutic biotarget for T-cell and antibody-mediated autoimmune diseases. RegRF is anti-idiotypic antibodies that have a shared paratope in addition to an individual paratope. Epitopes specific to the shared regRF paratope (regRF epitopes) can be obtained on conformers of IgG Fc fragments. Immunization with Fc fragments carrying regRF epitopes reduces rat collagen–induced arthritis and diminishes experimental autoimmune encephalomyelitis. The aim of this study was to determine whether IgG Fc fragments bearing regRF epitopes suppress experimental autoimmune thyroiditis (EAT). Four weeks after EAT induction, rats were immunized with IgG Fc fragments exhibiting regRF epitopes. Histology studies of the thyroid were performed 4 weeks later. Thyroid function and other parameters were also evaluated. Treatment of rats with Fc fragments bearing regRF epitopes decreased the number of rats affected by EAT, significantly decreased the extent of thyroid damage, prevented thyroid metaplasia, and restored normal thyroid hormone production. Therefore, RegRF is a promising biotarget in autoimmune thyroiditis, and Fc fragments bearing regRF epitopes are a potential therapeutic agent for that condition.</description><subject>Allergology</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Antigens</subject><subject>Arthritis</subject><subject>Autoimmune diseases</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>CD4 antigen</subject><subject>Chemical compounds</subject><subject>Collagen</subject><subject>Cytotoxicity</subject><subject>Damage prevention</subject><subject>Disease Models, Animal</subject><subject>Epitopes</subject><subject>Experimental allergic encephalomyelitis</subject><subject>Experimental autoimmune thyroiditis</subject><subject>Fragments</subject><subject>Hashimoto Disease - immunology</subject><subject>Hashimoto Disease - therapy</subject><subject>Histology</subject><subject>Immunization</subject><subject>Immunoglobulin Fc Fragments - therapeutic use</subject><subject>Immunoglobulin G</subject><subject>Immunology</subject><subject>Immunoregulation</subject><subject>Internal Medicine</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Medicine/Public Health</subject><subject>Metaplasia</subject><subject>Original Article</subject><subject>Pharmacology</subject><subject>Rats</subject><subject>Rheumatoid factor</subject><subject>Rheumatoid Factor - immunology</subject><subject>Thyroid</subject><subject>Thyroid gland</subject><subject>Thyroiditis</subject><subject>Thyroiditis, Autoimmune - therapy</subject><issn>0257-277X</issn><issn>1559-0755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kE1rGzEQhkVISFwnfyCHIsill21m9LGyjyHEqcEQCAkEchDyatZV8H5U2oX631eu0xZyKAgGxDPvvDyMXSJ8RQBznVCAKAsQooC5lKbAIzZBrecFGK2P2QSENoUw5uWMfUrpDQBLpeQpO5OlVGpWqgl7fSQ_VkPoWh5aTj97iqGhdnBb7sahC00ztsSH77vYBR-GkPh6x5ebe76oeB3dZs_mP3IxtBseafO44NSHoespnbOT2m0TXbzPKXte3D3dfitWD_fL25tVUUk5G4rcyWuQtSYhagdUaSNBqbV0c4FzjeSrClF5o1CshXSolAaPMyDvEWqUU_blkNvH7sdIabBNSBVtt66lbkxWGKmwLGV-U3b1AX3rxtjmdpkqS6FnQppMiQNVxS6lSLXtsxUXdxbB7tXbg3qb1dvf6u2-xef36HHdkP-78sd1BuQBSP1eFsV_t_8T-wstOI3s</recordid><startdate>20230201</startdate><enddate>20230201</enddate><creator>Beduleva, Liubov</creator><creator>Sidorov, Alexandr</creator><creator>Terentiev, Alexey</creator><creator>Varaksin, Viktor</creator><creator>Fomina, Kseniya</creator><creator>Menshikov, Igor</creator><general>Springer US</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7T5</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-2515-5960</orcidid></search><sort><creationdate>20230201</creationdate><title>Reduction in experimental autoimmune thyroiditis by IgG Fc fragments bearing regRF epitopes</title><author>Beduleva, Liubov ; Sidorov, Alexandr ; Terentiev, Alexey ; Varaksin, Viktor ; Fomina, Kseniya ; Menshikov, Igor</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c338t-644d503f5e22fa0ec573044b3a921951edcc114d7412b23a14450d180edd10f13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Allergology</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Antigens</topic><topic>Arthritis</topic><topic>Autoimmune diseases</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>CD4 antigen</topic><topic>Chemical compounds</topic><topic>Collagen</topic><topic>Cytotoxicity</topic><topic>Damage prevention</topic><topic>Disease Models, Animal</topic><topic>Epitopes</topic><topic>Experimental allergic encephalomyelitis</topic><topic>Experimental autoimmune thyroiditis</topic><topic>Fragments</topic><topic>Hashimoto Disease - immunology</topic><topic>Hashimoto Disease - therapy</topic><topic>Histology</topic><topic>Immunization</topic><topic>Immunoglobulin Fc Fragments - therapeutic use</topic><topic>Immunoglobulin G</topic><topic>Immunology</topic><topic>Immunoregulation</topic><topic>Internal Medicine</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Medicine/Public Health</topic><topic>Metaplasia</topic><topic>Original Article</topic><topic>Pharmacology</topic><topic>Rats</topic><topic>Rheumatoid factor</topic><topic>Rheumatoid Factor - immunology</topic><topic>Thyroid</topic><topic>Thyroid gland</topic><topic>Thyroiditis</topic><topic>Thyroiditis, Autoimmune - therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Beduleva, Liubov</creatorcontrib><creatorcontrib>Sidorov, Alexandr</creatorcontrib><creatorcontrib>Terentiev, Alexey</creatorcontrib><creatorcontrib>Varaksin, Viktor</creatorcontrib><creatorcontrib>Fomina, Kseniya</creatorcontrib><creatorcontrib>Menshikov, Igor</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</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>MEDLINE - Academic</collection><jtitle>Immunologic research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Beduleva, Liubov</au><au>Sidorov, Alexandr</au><au>Terentiev, Alexey</au><au>Varaksin, Viktor</au><au>Fomina, Kseniya</au><au>Menshikov, Igor</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduction in experimental autoimmune thyroiditis by IgG Fc fragments bearing regRF epitopes</atitle><jtitle>Immunologic research</jtitle><stitle>Immunol Res</stitle><addtitle>Immunol Res</addtitle><date>2023-02-01</date><risdate>2023</risdate><volume>71</volume><issue>1</issue><spage>83</spage><epage>91</epage><pages>83-91</pages><issn>0257-277X</issn><eissn>1559-0755</eissn><abstract>Previously, we identified a new immunoregulatory factor, the production of which provides rats with resistance to certain experimental autoimmune diseases. It has been named regulatory rheumatoid factor (regRF). RegRF inhibits the expansion of CD4 T lymphocytes by killing activated cells. CD4 T cells are essential for antibody production against a majority of antigens and for the generation of cytotoxic T cells; therefore, regRF is an attractive therapeutic biotarget for T-cell and antibody-mediated autoimmune diseases. RegRF is anti-idiotypic antibodies that have a shared paratope in addition to an individual paratope. Epitopes specific to the shared regRF paratope (regRF epitopes) can be obtained on conformers of IgG Fc fragments. Immunization with Fc fragments carrying regRF epitopes reduces rat collagen–induced arthritis and diminishes experimental autoimmune encephalomyelitis. The aim of this study was to determine whether IgG Fc fragments bearing regRF epitopes suppress experimental autoimmune thyroiditis (EAT). Four weeks after EAT induction, rats were immunized with IgG Fc fragments exhibiting regRF epitopes. Histology studies of the thyroid were performed 4 weeks later. Thyroid function and other parameters were also evaluated. Treatment of rats with Fc fragments bearing regRF epitopes decreased the number of rats affected by EAT, significantly decreased the extent of thyroid damage, prevented thyroid metaplasia, and restored normal thyroid hormone production. Therefore, RegRF is a promising biotarget in autoimmune thyroiditis, and Fc fragments bearing regRF epitopes are a potential therapeutic agent for that condition.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>36344864</pmid><doi>10.1007/s12026-022-09337-1</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-2515-5960</orcidid></addata></record> |
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| subjects | Allergology Animals Antibodies Antigens Arthritis Autoimmune diseases Biomedical and Life Sciences Biomedicine CD4 antigen Chemical compounds Collagen Cytotoxicity Damage prevention Disease Models, Animal Epitopes Experimental allergic encephalomyelitis Experimental autoimmune thyroiditis Fragments Hashimoto Disease - immunology Hashimoto Disease - therapy Histology Immunization Immunoglobulin Fc Fragments - therapeutic use Immunoglobulin G Immunology Immunoregulation Internal Medicine Lymphocytes Lymphocytes T Medicine/Public Health Metaplasia Original Article Pharmacology Rats Rheumatoid factor Rheumatoid Factor - immunology Thyroid Thyroid gland Thyroiditis Thyroiditis, Autoimmune - therapy |
| title | Reduction in experimental autoimmune thyroiditis by IgG Fc fragments bearing regRF epitopes |
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