Characterization of Regulatory B Cells in Graves' Disease and Hashimoto's Thyroiditis
A hallmark of regulatory B cells is IL-10 production, hence their designation as IL-10+ B cells. Little is known about the ability of self-antigens to induce IL-10+ B cells in Graves' disease (GD), Hashimoto's thyroiditis (HT), or other autoimmune disease. Here we pulsed purified B cells f...
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| description | A hallmark of regulatory B cells is IL-10 production, hence their designation as IL-10+ B cells. Little is known about the ability of self-antigens to induce IL-10+ B cells in Graves' disease (GD), Hashimoto's thyroiditis (HT), or other autoimmune disease. Here we pulsed purified B cells from 12 HT patients, 12 GD patients, and 12 healthy donors with the thyroid self-antigen, thyroglobulin (TG) and added the B cells back to the remaining peripheral blood mononuclear cells (PBMCs). This procedure induced IL-10+ B-cell differentiation in GD. A similar tendency was observed in healthy donors, but not in cells from patients with HT. In GD, B cells primed with TG induced IL-10-producing CD4+ T cells. To assess the maximal frequency of inducible IL-10+ B cells in the three donor groups PBMCs were stimulated with PMA/ionomycin. The resulting IL-10+ B-cell frequency was similar in the three groups and correlated with free T3 levels in GD patients. IL-10+ B cells from both patient groups displayed CD25 or TIM-1 more frequently than did those from healthy donors. B-cell expression of two surface marker combinations previously associated with regulatory B-cell functions, CD24hiCD38hi and CD27+CD43+, did not differ between patients and healthy donors. In conclusion, our findings indicate that autoimmune thyroiditis is not associated with reduced frequency of IL-10+ B cells. These results do not rule out regulatory B-cell dysfunction, however. The observed phenotypic differences between IL-10+ B cells from patients and healthy donors are discussed. |
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Little is known about the ability of self-antigens to induce IL-10+ B cells in Graves' disease (GD), Hashimoto's thyroiditis (HT), or other autoimmune disease. Here we pulsed purified B cells from 12 HT patients, 12 GD patients, and 12 healthy donors with the thyroid self-antigen, thyroglobulin (TG) and added the B cells back to the remaining peripheral blood mononuclear cells (PBMCs). This procedure induced IL-10+ B-cell differentiation in GD. A similar tendency was observed in healthy donors, but not in cells from patients with HT. In GD, B cells primed with TG induced IL-10-producing CD4+ T cells. To assess the maximal frequency of inducible IL-10+ B cells in the three donor groups PBMCs were stimulated with PMA/ionomycin. The resulting IL-10+ B-cell frequency was similar in the three groups and correlated with free T3 levels in GD patients. IL-10+ B cells from both patient groups displayed CD25 or TIM-1 more frequently than did those from healthy donors. B-cell expression of two surface marker combinations previously associated with regulatory B-cell functions, CD24hiCD38hi and CD27+CD43+, did not differ between patients and healthy donors. In conclusion, our findings indicate that autoimmune thyroiditis is not associated with reduced frequency of IL-10+ B cells. These results do not rule out regulatory B-cell dysfunction, however. The observed phenotypic differences between IL-10+ B cells from patients and healthy donors are discussed.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0127949</identifier><identifier>PMID: 26016954</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>ADP-ribosyl Cyclase 1 - immunology ; Adult ; Aged ; Antigens ; Arthritis ; Autoantigens ; Autoimmune Diseases - immunology ; Autoimmune thyroiditis ; B cells ; B-Lymphocytes, Regulatory - immunology ; Case-Control Studies ; CD24 Antigen - immunology ; CD25 antigen ; CD27 antigen ; CD4 antigen ; CD4-Positive T-Lymphocytes - immunology ; CD43 antigen ; Cell differentiation ; Cell surface ; Cytokines ; Development and progression ; Diabetes ; Endocrinology ; Female ; Graves Disease - immunology ; Graves' disease ; Hashimoto Disease - immunology ; Hepatitis A Virus Cellular Receptor 1 ; Hospitals ; Humans ; Infectious diseases ; Inflammation ; Interleukin 10 ; Interleukin-10 - immunology ; Interleukin-2 Receptor alpha Subunit - immunology ; Internal medicine ; Ionomycin ; Laboratory tests ; Leukocytes (mononuclear) ; Ligands ; Lymphocyte receptors ; Lymphocytes ; Lymphocytes B ; Lymphocytes T ; Male ; Membrane Glycoproteins - immunology ; Metabolism ; Middle Aged ; Patients ; Peripheral blood mononuclear cells ; Physiological aspects ; Receptors, Virus - immunology ; Rheumatology ; Surface markers ; T cell receptors ; Thyroglobulin ; Thyroglobulin - immunology ; Thyroid ; Thyroid gland ; Thyroid Gland - immunology ; Thyroiditis ; Triiodothyronine</subject><ispartof>PloS one, 2015-05, Vol.10 (5), p.e0127949-e0127949</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Kristensen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Kristensen et al 2015 Kristensen et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-1f0776148c46a45a534eb404106d0d11e3ce25572dfff1e0624f029c96a736dc3</citedby><cites>FETCH-LOGICAL-c692t-1f0776148c46a45a534eb404106d0d11e3ce25572dfff1e0624f029c96a736dc3</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/PMC4446335/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4446335/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23868,27926,27927,53793,53795</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26016954$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Richard, Yolande</contributor><creatorcontrib>Kristensen, Birte</creatorcontrib><creatorcontrib>Hegedüs, Laszlo</creatorcontrib><creatorcontrib>Lundy, Steven K</creatorcontrib><creatorcontrib>Brimnes, Marie K</creatorcontrib><creatorcontrib>Smith, Terry J</creatorcontrib><creatorcontrib>Nielsen, Claus H</creatorcontrib><title>Characterization of Regulatory B Cells in Graves' Disease and Hashimoto's Thyroiditis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>A hallmark of regulatory B cells is IL-10 production, hence their designation as IL-10+ B cells. Little is known about the ability of self-antigens to induce IL-10+ B cells in Graves' disease (GD), Hashimoto's thyroiditis (HT), or other autoimmune disease. Here we pulsed purified B cells from 12 HT patients, 12 GD patients, and 12 healthy donors with the thyroid self-antigen, thyroglobulin (TG) and added the B cells back to the remaining peripheral blood mononuclear cells (PBMCs). This procedure induced IL-10+ B-cell differentiation in GD. A similar tendency was observed in healthy donors, but not in cells from patients with HT. In GD, B cells primed with TG induced IL-10-producing CD4+ T cells. To assess the maximal frequency of inducible IL-10+ B cells in the three donor groups PBMCs were stimulated with PMA/ionomycin. The resulting IL-10+ B-cell frequency was similar in the three groups and correlated with free T3 levels in GD patients. IL-10+ B cells from both patient groups displayed CD25 or TIM-1 more frequently than did those from healthy donors. B-cell expression of two surface marker combinations previously associated with regulatory B-cell functions, CD24hiCD38hi and CD27+CD43+, did not differ between patients and healthy donors. In conclusion, our findings indicate that autoimmune thyroiditis is not associated with reduced frequency of IL-10+ B cells. These results do not rule out regulatory B-cell dysfunction, however. 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immunology</subject><subject>Hepatitis A Virus Cellular Receptor 1</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Infectious diseases</subject><subject>Inflammation</subject><subject>Interleukin 10</subject><subject>Interleukin-10 - immunology</subject><subject>Interleukin-2 Receptor alpha Subunit - immunology</subject><subject>Internal medicine</subject><subject>Ionomycin</subject><subject>Laboratory tests</subject><subject>Leukocytes (mononuclear)</subject><subject>Ligands</subject><subject>Lymphocyte receptors</subject><subject>Lymphocytes</subject><subject>Lymphocytes B</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Membrane Glycoproteins - immunology</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Patients</subject><subject>Peripheral blood mononuclear cells</subject><subject>Physiological aspects</subject><subject>Receptors, Virus - immunology</subject><subject>Rheumatology</subject><subject>Surface markers</subject><subject>T cell receptors</subject><subject>Thyroglobulin</subject><subject>Thyroglobulin - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kristensen, Birte</au><au>Hegedüs, Laszlo</au><au>Lundy, Steven K</au><au>Brimnes, Marie K</au><au>Smith, Terry J</au><au>Nielsen, Claus H</au><au>Richard, Yolande</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Characterization of Regulatory B Cells in Graves' Disease and Hashimoto's Thyroiditis</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-05-27</date><risdate>2015</risdate><volume>10</volume><issue>5</issue><spage>e0127949</spage><epage>e0127949</epage><pages>e0127949-e0127949</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>A hallmark of regulatory B cells is IL-10 production, hence their designation as IL-10+ B cells. Little is known about the ability of self-antigens to induce IL-10+ B cells in Graves' disease (GD), Hashimoto's thyroiditis (HT), or other autoimmune disease. Here we pulsed purified B cells from 12 HT patients, 12 GD patients, and 12 healthy donors with the thyroid self-antigen, thyroglobulin (TG) and added the B cells back to the remaining peripheral blood mononuclear cells (PBMCs). This procedure induced IL-10+ B-cell differentiation in GD. A similar tendency was observed in healthy donors, but not in cells from patients with HT. In GD, B cells primed with TG induced IL-10-producing CD4+ T cells. To assess the maximal frequency of inducible IL-10+ B cells in the three donor groups PBMCs were stimulated with PMA/ionomycin. The resulting IL-10+ B-cell frequency was similar in the three groups and correlated with free T3 levels in GD patients. IL-10+ B cells from both patient groups displayed CD25 or TIM-1 more frequently than did those from healthy donors. B-cell expression of two surface marker combinations previously associated with regulatory B-cell functions, CD24hiCD38hi and CD27+CD43+, did not differ between patients and healthy donors. In conclusion, our findings indicate that autoimmune thyroiditis is not associated with reduced frequency of IL-10+ B cells. These results do not rule out regulatory B-cell dysfunction, however. The observed phenotypic differences between IL-10+ B cells from patients and healthy donors are discussed.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26016954</pmid><doi>10.1371/journal.pone.0127949</doi><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1683578312 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | ADP-ribosyl Cyclase 1 - immunology Adult Aged Antigens Arthritis Autoantigens Autoimmune Diseases - immunology Autoimmune thyroiditis B cells B-Lymphocytes, Regulatory - immunology Case-Control Studies CD24 Antigen - immunology CD25 antigen CD27 antigen CD4 antigen CD4-Positive T-Lymphocytes - immunology CD43 antigen Cell differentiation Cell surface Cytokines Development and progression Diabetes Endocrinology Female Graves Disease - immunology Graves' disease Hashimoto Disease - immunology Hepatitis A Virus Cellular Receptor 1 Hospitals Humans Infectious diseases Inflammation Interleukin 10 Interleukin-10 - immunology Interleukin-2 Receptor alpha Subunit - immunology Internal medicine Ionomycin Laboratory tests Leukocytes (mononuclear) Ligands Lymphocyte receptors Lymphocytes Lymphocytes B Lymphocytes T Male Membrane Glycoproteins - immunology Metabolism Middle Aged Patients Peripheral blood mononuclear cells Physiological aspects Receptors, Virus - immunology Rheumatology Surface markers T cell receptors Thyroglobulin Thyroglobulin - immunology Thyroid Thyroid gland Thyroid Gland - immunology Thyroiditis Triiodothyronine |
| title | Characterization of Regulatory B Cells in Graves' Disease and Hashimoto's Thyroiditis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-18T11%3A16%3A33IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Characterization%20of%20Regulatory%20B%20Cells%20in%20Graves'%20Disease%20and%20Hashimoto's%20Thyroiditis&rft.jtitle=PloS%20one&rft.au=Kristensen,%20Birte&rft.date=2015-05-27&rft.volume=10&rft.issue=5&rft.spage=e0127949&rft.epage=e0127949&rft.pages=e0127949-e0127949&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0127949&rft_dat=%3Cgale_plos_%3EA432405158%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1683578312&rft_id=info:pmid/26016954&rft_galeid=A432405158&rft_doaj_id=oai_doaj_org_article_b6972b3b28f14e97b01c185142be5e43&rfr_iscdi=true |