The pathogenic role of circulating Hashimoto's Thyroiditis‐derived TPO‐positive IgG on fetal loss in naïve mice
Problem Antibody‐mediated autoimmune diseases, such as autoimmune thyroid diseases (ATD), systemic lupus erythematosus (SLE), and antiphospholipid syndrome (APS), often are associated with recurrent fetal loss. One of the ATD is Hashimoto's thyroiditis which recently showed association with com...
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| Veröffentlicht in: | American journal of reproductive immunology (1989) 2021-01, Vol.85 (1), p.e13331-n/a |
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| container_title | American journal of reproductive immunology (1989) |
| container_volume | 85 |
| creator | Borodina, Elena Katz, Itai Antonelli, Alessandro Gzgzyan, Alexander M. Dzhemlikhanova, Liailia Kh Ostrinski, Yuri Niauri, Dariko Khizroeva, Jamilya Bitsadze, Victoria Makatsariya, Alexander Tincani, Angela Nalli, Cecilia Churilov, Leonid P. Shovman, Ora Halpert, Gilad Blank, Miri Shoenfeld, Yehuda Amital, Howard |
| description | Problem
Antibody‐mediated autoimmune diseases, such as autoimmune thyroid diseases (ATD), systemic lupus erythematosus (SLE), and antiphospholipid syndrome (APS), often are associated with recurrent fetal loss. One of the ATD is Hashimoto's thyroiditis which recently showed association with complications of pregnancy with increased levels of circulating autoantibodies reactive with epitopes on thyroid tissue such as thyroid peroxidase (anti‐TPO). In retrospective study of sera analyses in patients with Hashimoto's thyroiditis, all patients had mainly elevated circulating anti‐TPO autoantibodies.
Aim
We assessed the potential of human anti‐TPO highly positive IgG, derived from patients with Hashimoto's thyroiditis sera associated with complications of pregnancy, to cause directly complications of pregnancy in murine model.
Method of study
Naïve ICR female mice, infused intravenously with 100 μg of anti‐TPO‐positive IgG, showed increased fetal loss and embryo small for date (P |
| doi_str_mv | 10.1111/aji.13331 |
| format | Article |
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Antibody‐mediated autoimmune diseases, such as autoimmune thyroid diseases (ATD), systemic lupus erythematosus (SLE), and antiphospholipid syndrome (APS), often are associated with recurrent fetal loss. One of the ATD is Hashimoto's thyroiditis which recently showed association with complications of pregnancy with increased levels of circulating autoantibodies reactive with epitopes on thyroid tissue such as thyroid peroxidase (anti‐TPO). In retrospective study of sera analyses in patients with Hashimoto's thyroiditis, all patients had mainly elevated circulating anti‐TPO autoantibodies.
Aim
We assessed the potential of human anti‐TPO highly positive IgG, derived from patients with Hashimoto's thyroiditis sera associated with complications of pregnancy, to cause directly complications of pregnancy in murine model.
Method of study
Naïve ICR female mice, infused intravenously with 100 μg of anti‐TPO‐positive IgG, showed increased fetal loss and embryo small for date (P < .001) in comparison with mice passively transferred with commercial IgG or PBS. Moreover, we observed embryos small for date in the mice passively transferred with anti‐TPO‐positive IgG, exemplified by reduced weight of embryos and placentae (P = .001). Histopathological examination revealed delay in fetal development in 50% cases of anti‐TPO‐positive IgG‐treated mice. Importantly, pathological changes in the transition zone, state of glycogen cells, and significant structural changes in the labyrinth part of placenta were observed in all anti‐TPO‐positive IgG samples.
Conclusion
The current study shows in the first time, a direct proof of concept, on the association of human TPO‐positive IgG from Hashimoto's thyroiditis patients on fetal loss induction in murine model.</description><identifier>ISSN: 1046-7408</identifier><identifier>EISSN: 1600-0897</identifier><identifier>DOI: 10.1111/aji.13331</identifier><identifier>PMID: 32893404</identifier><language>eng</language><publisher>Denmark: Wiley Subscription Services, Inc</publisher><subject>Animal models ; Animals ; Antiphospholipid syndrome ; anti‐TPO ; Autoantibodies ; Autoantibodies - immunology ; Autoantigens - immunology ; Autoimmune diseases ; Embryos ; Epitopes ; Female ; Fetal Death ; Fetuses ; Glycogen ; Hashimoto Disease - blood ; Hashimoto Disease - immunology ; Hashimoto's thyroiditis ; Humans ; Immunoglobulin G ; Immunoglobulin G - immunology ; Iodide peroxidase ; Iodide Peroxidase - immunology ; Iron-Binding Proteins - immunology ; Mice ; Mice, Inbred ICR ; murine fetal loss ; Placenta ; Placenta - pathology ; Pregnancy ; Pregnancy complications ; Pregnancy Complications - immunology ; reproductive failure ; Systemic lupus erythematosus ; Thyroid diseases ; Thyroid gland ; Thyroiditis</subject><ispartof>American journal of reproductive immunology (1989), 2021-01, Vol.85 (1), p.e13331-n/a</ispartof><rights>2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><rights>2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.</rights><rights>Copyright © 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3531-114e4ed947297b7b8fa894985e8daff31f4ae4199894bbca0d327c2f4e6659fb3</citedby><cites>FETCH-LOGICAL-c3531-114e4ed947297b7b8fa894985e8daff31f4ae4199894bbca0d327c2f4e6659fb3</cites><orcidid>0000-0002-7801-7123 ; 0000-0002-5610-7347 ; 0000-0002-0725-9686 ; 0000-0001-8404-1042</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Faji.13331$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Faji.13331$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32893404$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Borodina, Elena</creatorcontrib><creatorcontrib>Katz, Itai</creatorcontrib><creatorcontrib>Antonelli, Alessandro</creatorcontrib><creatorcontrib>Gzgzyan, Alexander M.</creatorcontrib><creatorcontrib>Dzhemlikhanova, Liailia Kh</creatorcontrib><creatorcontrib>Ostrinski, Yuri</creatorcontrib><creatorcontrib>Niauri, Dariko</creatorcontrib><creatorcontrib>Khizroeva, Jamilya</creatorcontrib><creatorcontrib>Bitsadze, Victoria</creatorcontrib><creatorcontrib>Makatsariya, Alexander</creatorcontrib><creatorcontrib>Tincani, Angela</creatorcontrib><creatorcontrib>Nalli, Cecilia</creatorcontrib><creatorcontrib>Churilov, Leonid P.</creatorcontrib><creatorcontrib>Shovman, Ora</creatorcontrib><creatorcontrib>Halpert, Gilad</creatorcontrib><creatorcontrib>Blank, Miri</creatorcontrib><creatorcontrib>Shoenfeld, Yehuda</creatorcontrib><creatorcontrib>Amital, Howard</creatorcontrib><title>The pathogenic role of circulating Hashimoto's Thyroiditis‐derived TPO‐positive IgG on fetal loss in naïve mice</title><title>American journal of reproductive immunology (1989)</title><addtitle>Am J Reprod Immunol</addtitle><description>Problem
Antibody‐mediated autoimmune diseases, such as autoimmune thyroid diseases (ATD), systemic lupus erythematosus (SLE), and antiphospholipid syndrome (APS), often are associated with recurrent fetal loss. One of the ATD is Hashimoto's thyroiditis which recently showed association with complications of pregnancy with increased levels of circulating autoantibodies reactive with epitopes on thyroid tissue such as thyroid peroxidase (anti‐TPO). In retrospective study of sera analyses in patients with Hashimoto's thyroiditis, all patients had mainly elevated circulating anti‐TPO autoantibodies.
Aim
We assessed the potential of human anti‐TPO highly positive IgG, derived from patients with Hashimoto's thyroiditis sera associated with complications of pregnancy, to cause directly complications of pregnancy in murine model.
Method of study
Naïve ICR female mice, infused intravenously with 100 μg of anti‐TPO‐positive IgG, showed increased fetal loss and embryo small for date (P < .001) in comparison with mice passively transferred with commercial IgG or PBS. Moreover, we observed embryos small for date in the mice passively transferred with anti‐TPO‐positive IgG, exemplified by reduced weight of embryos and placentae (P = .001). Histopathological examination revealed delay in fetal development in 50% cases of anti‐TPO‐positive IgG‐treated mice. Importantly, pathological changes in the transition zone, state of glycogen cells, and significant structural changes in the labyrinth part of placenta were observed in all anti‐TPO‐positive IgG samples.
Conclusion
The current study shows in the first time, a direct proof of concept, on the association of human TPO‐positive IgG from Hashimoto's thyroiditis patients on fetal loss induction in murine model.</description><subject>Animal models</subject><subject>Animals</subject><subject>Antiphospholipid syndrome</subject><subject>anti‐TPO</subject><subject>Autoantibodies</subject><subject>Autoantibodies - immunology</subject><subject>Autoantigens - immunology</subject><subject>Autoimmune diseases</subject><subject>Embryos</subject><subject>Epitopes</subject><subject>Female</subject><subject>Fetal Death</subject><subject>Fetuses</subject><subject>Glycogen</subject><subject>Hashimoto Disease - blood</subject><subject>Hashimoto Disease - immunology</subject><subject>Hashimoto's thyroiditis</subject><subject>Humans</subject><subject>Immunoglobulin G</subject><subject>Immunoglobulin G - immunology</subject><subject>Iodide peroxidase</subject><subject>Iodide Peroxidase - immunology</subject><subject>Iron-Binding Proteins - immunology</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>murine fetal loss</subject><subject>Placenta</subject><subject>Placenta - pathology</subject><subject>Pregnancy</subject><subject>Pregnancy complications</subject><subject>Pregnancy Complications - immunology</subject><subject>reproductive failure</subject><subject>Systemic lupus erythematosus</subject><subject>Thyroid diseases</subject><subject>Thyroid gland</subject><subject>Thyroiditis</subject><issn>1046-7408</issn><issn>1600-0897</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kcFO3DAQhq2qqFDaQ18AWeoBOATs2BvHxxUqsBUSPWzPkeOMd71K4sVOQHvrI_AmPETfhCdh6FIOSPgy49-ffo3nJ-QbZyccz6lZ-RMuhOAfyB4vGMtYqdVH7JksMiVZuUs-p7RiDHWhPpFdkWMjmdwjw3wJdG2GZVhA7y2NoQUaHLU-2rE1g-8X9NKkpe_CEA4TnS83MfjGDz49_rlvIPpbaOj81zXe1iGhfgt0trigoacOBtPSNqREfU978_cB3zpv4QvZcaZN8PWl7pPf5z_mZ5fZ1fXF7Gx6lVkxETzjXIKERkuVa1WrunSm1FKXEygb45zgThqQXGtU69oa1ohc2dxJKIqJdrXYJ0db33UMNyOkoep8stC2pocwpiqXkhWF4loi-v0Nugpj7HE6pEqOyEQVSB1vKRvxVxFctY6-M3FTcVY9R1FhFNW_KJA9eHEc6w6aV_L_7hE43QJ3voXN-07V9Odsa_kE8IWVLQ</recordid><startdate>202101</startdate><enddate>202101</enddate><creator>Borodina, Elena</creator><creator>Katz, Itai</creator><creator>Antonelli, Alessandro</creator><creator>Gzgzyan, Alexander M.</creator><creator>Dzhemlikhanova, Liailia Kh</creator><creator>Ostrinski, Yuri</creator><creator>Niauri, Dariko</creator><creator>Khizroeva, Jamilya</creator><creator>Bitsadze, Victoria</creator><creator>Makatsariya, Alexander</creator><creator>Tincani, Angela</creator><creator>Nalli, Cecilia</creator><creator>Churilov, Leonid P.</creator><creator>Shovman, Ora</creator><creator>Halpert, Gilad</creator><creator>Blank, Miri</creator><creator>Shoenfeld, Yehuda</creator><creator>Amital, Howard</creator><general>Wiley Subscription Services, Inc</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>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7801-7123</orcidid><orcidid>https://orcid.org/0000-0002-5610-7347</orcidid><orcidid>https://orcid.org/0000-0002-0725-9686</orcidid><orcidid>https://orcid.org/0000-0001-8404-1042</orcidid></search><sort><creationdate>202101</creationdate><title>The pathogenic role of circulating Hashimoto's Thyroiditis‐derived TPO‐positive IgG on fetal loss in naïve mice</title><author>Borodina, Elena ; Katz, Itai ; Antonelli, Alessandro ; Gzgzyan, Alexander M. ; Dzhemlikhanova, Liailia Kh ; Ostrinski, Yuri ; Niauri, Dariko ; Khizroeva, Jamilya ; Bitsadze, Victoria ; Makatsariya, Alexander ; Tincani, Angela ; Nalli, Cecilia ; Churilov, Leonid P. ; Shovman, Ora ; Halpert, Gilad ; Blank, Miri ; Shoenfeld, Yehuda ; Amital, Howard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3531-114e4ed947297b7b8fa894985e8daff31f4ae4199894bbca0d327c2f4e6659fb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animal models</topic><topic>Animals</topic><topic>Antiphospholipid syndrome</topic><topic>anti‐TPO</topic><topic>Autoantibodies</topic><topic>Autoantibodies - immunology</topic><topic>Autoantigens - immunology</topic><topic>Autoimmune diseases</topic><topic>Embryos</topic><topic>Epitopes</topic><topic>Female</topic><topic>Fetal Death</topic><topic>Fetuses</topic><topic>Glycogen</topic><topic>Hashimoto Disease - blood</topic><topic>Hashimoto Disease - immunology</topic><topic>Hashimoto's thyroiditis</topic><topic>Humans</topic><topic>Immunoglobulin G</topic><topic>Immunoglobulin G - immunology</topic><topic>Iodide peroxidase</topic><topic>Iodide Peroxidase - immunology</topic><topic>Iron-Binding Proteins - immunology</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>murine fetal loss</topic><topic>Placenta</topic><topic>Placenta - pathology</topic><topic>Pregnancy</topic><topic>Pregnancy complications</topic><topic>Pregnancy Complications - immunology</topic><topic>reproductive failure</topic><topic>Systemic lupus erythematosus</topic><topic>Thyroid diseases</topic><topic>Thyroid gland</topic><topic>Thyroiditis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Borodina, Elena</creatorcontrib><creatorcontrib>Katz, Itai</creatorcontrib><creatorcontrib>Antonelli, Alessandro</creatorcontrib><creatorcontrib>Gzgzyan, Alexander M.</creatorcontrib><creatorcontrib>Dzhemlikhanova, Liailia Kh</creatorcontrib><creatorcontrib>Ostrinski, Yuri</creatorcontrib><creatorcontrib>Niauri, Dariko</creatorcontrib><creatorcontrib>Khizroeva, Jamilya</creatorcontrib><creatorcontrib>Bitsadze, Victoria</creatorcontrib><creatorcontrib>Makatsariya, Alexander</creatorcontrib><creatorcontrib>Tincani, Angela</creatorcontrib><creatorcontrib>Nalli, Cecilia</creatorcontrib><creatorcontrib>Churilov, Leonid P.</creatorcontrib><creatorcontrib>Shovman, Ora</creatorcontrib><creatorcontrib>Halpert, Gilad</creatorcontrib><creatorcontrib>Blank, Miri</creatorcontrib><creatorcontrib>Shoenfeld, Yehuda</creatorcontrib><creatorcontrib>Amital, Howard</creatorcontrib><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>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of reproductive immunology (1989)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Borodina, Elena</au><au>Katz, Itai</au><au>Antonelli, Alessandro</au><au>Gzgzyan, Alexander M.</au><au>Dzhemlikhanova, Liailia Kh</au><au>Ostrinski, Yuri</au><au>Niauri, Dariko</au><au>Khizroeva, Jamilya</au><au>Bitsadze, Victoria</au><au>Makatsariya, Alexander</au><au>Tincani, Angela</au><au>Nalli, Cecilia</au><au>Churilov, Leonid P.</au><au>Shovman, Ora</au><au>Halpert, Gilad</au><au>Blank, Miri</au><au>Shoenfeld, Yehuda</au><au>Amital, Howard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The pathogenic role of circulating Hashimoto's Thyroiditis‐derived TPO‐positive IgG on fetal loss in naïve mice</atitle><jtitle>American journal of reproductive immunology (1989)</jtitle><addtitle>Am J Reprod Immunol</addtitle><date>2021-01</date><risdate>2021</risdate><volume>85</volume><issue>1</issue><spage>e13331</spage><epage>n/a</epage><pages>e13331-n/a</pages><issn>1046-7408</issn><eissn>1600-0897</eissn><abstract>Problem
Antibody‐mediated autoimmune diseases, such as autoimmune thyroid diseases (ATD), systemic lupus erythematosus (SLE), and antiphospholipid syndrome (APS), often are associated with recurrent fetal loss. One of the ATD is Hashimoto's thyroiditis which recently showed association with complications of pregnancy with increased levels of circulating autoantibodies reactive with epitopes on thyroid tissue such as thyroid peroxidase (anti‐TPO). In retrospective study of sera analyses in patients with Hashimoto's thyroiditis, all patients had mainly elevated circulating anti‐TPO autoantibodies.
Aim
We assessed the potential of human anti‐TPO highly positive IgG, derived from patients with Hashimoto's thyroiditis sera associated with complications of pregnancy, to cause directly complications of pregnancy in murine model.
Method of study
Naïve ICR female mice, infused intravenously with 100 μg of anti‐TPO‐positive IgG, showed increased fetal loss and embryo small for date (P < .001) in comparison with mice passively transferred with commercial IgG or PBS. Moreover, we observed embryos small for date in the mice passively transferred with anti‐TPO‐positive IgG, exemplified by reduced weight of embryos and placentae (P = .001). Histopathological examination revealed delay in fetal development in 50% cases of anti‐TPO‐positive IgG‐treated mice. Importantly, pathological changes in the transition zone, state of glycogen cells, and significant structural changes in the labyrinth part of placenta were observed in all anti‐TPO‐positive IgG samples.
Conclusion
The current study shows in the first time, a direct proof of concept, on the association of human TPO‐positive IgG from Hashimoto's thyroiditis patients on fetal loss induction in murine model.</abstract><cop>Denmark</cop><pub>Wiley Subscription Services, Inc</pub><pmid>32893404</pmid><doi>10.1111/aji.13331</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-7801-7123</orcidid><orcidid>https://orcid.org/0000-0002-5610-7347</orcidid><orcidid>https://orcid.org/0000-0002-0725-9686</orcidid><orcidid>https://orcid.org/0000-0001-8404-1042</orcidid></addata></record> |
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| identifier | ISSN: 1046-7408 |
| ispartof | American journal of reproductive immunology (1989), 2021-01, Vol.85 (1), p.e13331-n/a |
| issn | 1046-7408 1600-0897 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2440667194 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Animal models Animals Antiphospholipid syndrome anti‐TPO Autoantibodies Autoantibodies - immunology Autoantigens - immunology Autoimmune diseases Embryos Epitopes Female Fetal Death Fetuses Glycogen Hashimoto Disease - blood Hashimoto Disease - immunology Hashimoto's thyroiditis Humans Immunoglobulin G Immunoglobulin G - immunology Iodide peroxidase Iodide Peroxidase - immunology Iron-Binding Proteins - immunology Mice Mice, Inbred ICR murine fetal loss Placenta Placenta - pathology Pregnancy Pregnancy complications Pregnancy Complications - immunology reproductive failure Systemic lupus erythematosus Thyroid diseases Thyroid gland Thyroiditis |
| title | The pathogenic role of circulating Hashimoto's Thyroiditis‐derived TPO‐positive IgG on fetal loss in naïve mice |
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