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Aberrant expression of interleukin-10 and activation-induced cytidine deaminase in B cells from patients with Behçet's disease
Despite extensive studies, the pathogenesis of Behçet's disease (BD) remains unclear. In particular, the roles of B cells in patients with BD have not been elucidated. Activation-induced cytidine deaminase (AID) is a critical enzyme for immunoglobulin (Ig) heavy chain class switching and somati...
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Published in: | Biomedical reports 2017-12, Vol.7 (6), p.520-526 |
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description | Despite extensive studies, the pathogenesis of Behçet's disease (BD) remains unclear. In particular, the roles of B cells in patients with BD have not been elucidated. Activation-induced cytidine deaminase (AID) is a critical enzyme for immunoglobulin (Ig) heavy chain class switching and somatic hypermutation in B cells and the abnormal expression of AID in various immune conditions has previously been studied. B10 cells, an interleukin (IL)-10-secreting subset of regulatory B cells, function to downregulate inflammation and autoimmunity. Thus, in the present study, the relevance of B cells in patients with BD was investigated. The plasma levels of IL-10 and IgA and the proportions of cluster of differentiation (CD)43+ B cells, excluding naïve B cells, were measured in 16 patients with BD and 16 age- and sex-matched healthy controls (HCs). Additionally, the mRNA levels of IL-10 and AID were assessed in B cells from fresh peripheral blood samples of the BD patients and HCs. The plasma level of IL-10 in patients with BD did not differ significantly from that in HCs. Similarly, there was no significant difference in the plasma level of IgA, although a slight increase was observed in patients with BD compared with that in HCs. There were no differences in CD43+CD19+ B cell numbers between patients with BD and HCs. However, IL-10 mRNA levels were significantly reduced (P |
doi_str_mv | 10.3892/br.2017.996 |
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In particular, the roles of B cells in patients with BD have not been elucidated. Activation-induced cytidine deaminase (AID) is a critical enzyme for immunoglobulin (Ig) heavy chain class switching and somatic hypermutation in B cells and the abnormal expression of AID in various immune conditions has previously been studied. B10 cells, an interleukin (IL)-10-secreting subset of regulatory B cells, function to downregulate inflammation and autoimmunity. Thus, in the present study, the relevance of B cells in patients with BD was investigated. The plasma levels of IL-10 and IgA and the proportions of cluster of differentiation (CD)43+ B cells, excluding naïve B cells, were measured in 16 patients with BD and 16 age- and sex-matched healthy controls (HCs). Additionally, the mRNA levels of IL-10 and AID were assessed in B cells from fresh peripheral blood samples of the BD patients and HCs. The plasma level of IL-10 in patients with BD did not differ significantly from that in HCs. Similarly, there was no significant difference in the plasma level of IgA, although a slight increase was observed in patients with BD compared with that in HCs. There were no differences in CD43+CD19+ B cell numbers between patients with BD and HCs. However, IL-10 mRNA levels were significantly reduced (P<0.05), while AID mRNA levels were significantly increased (P<0.01) in the B cells of patients with BD compared with those in HCs. These results provide insight into the role of B cells in patients with BD.</description><identifier>ISSN: 2049-9434</identifier><identifier>EISSN: 2049-9442</identifier><identifier>DOI: 10.3892/br.2017.996</identifier><identifier>PMID: 29188055</identifier><language>eng</language><publisher>England: D.A. Spandidos</publisher><subject>Aberration ; Activation-induced cytidine deaminase ; Autoimmunity ; B cells ; Behcet's syndrome ; Behçet's disease ; CD19 antigen ; CD43 antigen ; Cell activation ; Class switching ; cluster of differentiation 43 ; Cytidine deaminase ; Enzyme-linked immunosorbent assay ; Enzymes ; Fluorescein ; Immunoglobulin A ; Inflammation ; Interleukin 10 ; Interleukins ; Lupus ; Lymphocyte receptors ; Lymphocytes ; Lymphocytes B ; Medical research ; mRNA ; Pathogenesis ; Patients ; Peripheral blood ; Plasma levels ; RNA ; Somatic hypermutation ; Somatotropin ; Studies ; Systemic lupus erythematosus ; T cell receptors</subject><ispartof>Biomedical reports, 2017-12, Vol.7 (6), p.520-526</ispartof><rights>Copyright: © Yoon et al.</rights><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><rights>Copyright: © Yoon et al. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5702955/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5702955/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29188055$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoon, Jeong-Yun</creatorcontrib><creatorcontrib>Lee, Yeojin</creatorcontrib><creatorcontrib>Yu, Seong-Lan</creatorcontrib><creatorcontrib>Yoon, Hee-Kyung</creatorcontrib><creatorcontrib>Park, Ha-Yan</creatorcontrib><creatorcontrib>Joung, Chung-Il</creatorcontrib><creatorcontrib>Park, Seok-Rae</creatorcontrib><creatorcontrib>Kwon, Mihye</creatorcontrib><creatorcontrib>Kang, Jaeku</creatorcontrib><title>Aberrant expression of interleukin-10 and activation-induced cytidine deaminase in B cells from patients with Behçet's disease</title><title>Biomedical reports</title><addtitle>Biomed Rep</addtitle><description>Despite extensive studies, the pathogenesis of Behçet's disease (BD) remains unclear. In particular, the roles of B cells in patients with BD have not been elucidated. Activation-induced cytidine deaminase (AID) is a critical enzyme for immunoglobulin (Ig) heavy chain class switching and somatic hypermutation in B cells and the abnormal expression of AID in various immune conditions has previously been studied. B10 cells, an interleukin (IL)-10-secreting subset of regulatory B cells, function to downregulate inflammation and autoimmunity. Thus, in the present study, the relevance of B cells in patients with BD was investigated. The plasma levels of IL-10 and IgA and the proportions of cluster of differentiation (CD)43+ B cells, excluding naïve B cells, were measured in 16 patients with BD and 16 age- and sex-matched healthy controls (HCs). Additionally, the mRNA levels of IL-10 and AID were assessed in B cells from fresh peripheral blood samples of the BD patients and HCs. The plasma level of IL-10 in patients with BD did not differ significantly from that in HCs. Similarly, there was no significant difference in the plasma level of IgA, although a slight increase was observed in patients with BD compared with that in HCs. There were no differences in CD43+CD19+ B cell numbers between patients with BD and HCs. However, IL-10 mRNA levels were significantly reduced (P<0.05), while AID mRNA levels were significantly increased (P<0.01) in the B cells of patients with BD compared with those in HCs. These results provide insight into the role of B cells in patients with BD.</description><subject>Aberration</subject><subject>Activation-induced cytidine deaminase</subject><subject>Autoimmunity</subject><subject>B cells</subject><subject>Behcet's syndrome</subject><subject>Behçet's disease</subject><subject>CD19 antigen</subject><subject>CD43 antigen</subject><subject>Cell activation</subject><subject>Class switching</subject><subject>cluster of differentiation 43</subject><subject>Cytidine deaminase</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Enzymes</subject><subject>Fluorescein</subject><subject>Immunoglobulin A</subject><subject>Inflammation</subject><subject>Interleukin 10</subject><subject>Interleukins</subject><subject>Lupus</subject><subject>Lymphocyte receptors</subject><subject>Lymphocytes</subject><subject>Lymphocytes B</subject><subject>Medical research</subject><subject>mRNA</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>Peripheral blood</subject><subject>Plasma levels</subject><subject>RNA</subject><subject>Somatic hypermutation</subject><subject>Somatotropin</subject><subject>Studies</subject><subject>Systemic lupus erythematosus</subject><subject>T cell receptors</subject><issn>2049-9434</issn><issn>2049-9442</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNptks9uFSEUxidGY5valXtD4kI3c-XPwMDG5N5Gq0kTE6PrCQNn7qXOwAhMtSsfxwfxxcqN9dYaOQsI_M53-A5U1VOCV0wq-qqPK4pJu1JKPKiOKW5UrZqGPjysWXNUnaZ0ictQLaZcPq6OqCJSYs6Pqx_rHmLUPiP4PkdIyQWPwoCczxBHWL44XxOMtLdIm-yudC5A7bxdDFhkrrOzzgOyoCfndYKSiDbIwDgmNMQwoblkgM8JfXN5hzaw-_UT8ouErEtQ-CfVo0GPCU5v55Pq89s3n87e1Rcfzt-frS_qbbGZa9rjnjTc6J4orDSTGjA2FBrBOR2oMLoVQDluySAl2IH3fS9YqxhtCBG4ZSfV69-689JPYE25UtRjN0c36XjdBe26-yfe7bptuOp46ZnivAi8vBWI4esCKXeTS3uf2kNYUkdKcwVVjWAFff4PehmW6Iu9QkkhBKNS3VFbPULn_BBKXbMX7da8WJGE8T21-g9VwsLkTPAwuLJ_L-HZ30YPDv88-V3dNJdXdTakA7P5WOMS5S-xG-WsueY</recordid><startdate>20171201</startdate><enddate>20171201</enddate><creator>Yoon, Jeong-Yun</creator><creator>Lee, Yeojin</creator><creator>Yu, Seong-Lan</creator><creator>Yoon, Hee-Kyung</creator><creator>Park, Ha-Yan</creator><creator>Joung, Chung-Il</creator><creator>Park, Seok-Rae</creator><creator>Kwon, Mihye</creator><creator>Kang, Jaeku</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20171201</creationdate><title>Aberrant expression of interleukin-10 and activation-induced cytidine deaminase in B cells from patients with Behçet's disease</title><author>Yoon, Jeong-Yun ; Lee, Yeojin ; Yu, Seong-Lan ; Yoon, Hee-Kyung ; Park, Ha-Yan ; Joung, Chung-Il ; Park, Seok-Rae ; Kwon, Mihye ; Kang, Jaeku</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g389t-2b0b145cab1909a38ae00c2e46552f26ca76e25071f88edf5bbb6379324116073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Aberration</topic><topic>Activation-induced cytidine deaminase</topic><topic>Autoimmunity</topic><topic>B cells</topic><topic>Behcet's syndrome</topic><topic>Behçet's disease</topic><topic>CD19 antigen</topic><topic>CD43 antigen</topic><topic>Cell activation</topic><topic>Class switching</topic><topic>cluster of differentiation 43</topic><topic>Cytidine deaminase</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Enzymes</topic><topic>Fluorescein</topic><topic>Immunoglobulin A</topic><topic>Inflammation</topic><topic>Interleukin 10</topic><topic>Interleukins</topic><topic>Lupus</topic><topic>Lymphocyte receptors</topic><topic>Lymphocytes</topic><topic>Lymphocytes B</topic><topic>Medical research</topic><topic>mRNA</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>Peripheral blood</topic><topic>Plasma levels</topic><topic>RNA</topic><topic>Somatic hypermutation</topic><topic>Somatotropin</topic><topic>Studies</topic><topic>Systemic lupus erythematosus</topic><topic>T cell receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoon, Jeong-Yun</creatorcontrib><creatorcontrib>Lee, Yeojin</creatorcontrib><creatorcontrib>Yu, Seong-Lan</creatorcontrib><creatorcontrib>Yoon, Hee-Kyung</creatorcontrib><creatorcontrib>Park, Ha-Yan</creatorcontrib><creatorcontrib>Joung, Chung-Il</creatorcontrib><creatorcontrib>Park, Seok-Rae</creatorcontrib><creatorcontrib>Kwon, Mihye</creatorcontrib><creatorcontrib>Kang, Jaeku</creatorcontrib><collection>PubMed</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>ProQuest Biological Science Journals</collection><collection>ProQuest advanced technologies & aerospace journals</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Biomedical reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yoon, Jeong-Yun</au><au>Lee, Yeojin</au><au>Yu, Seong-Lan</au><au>Yoon, Hee-Kyung</au><au>Park, Ha-Yan</au><au>Joung, Chung-Il</au><au>Park, Seok-Rae</au><au>Kwon, Mihye</au><au>Kang, Jaeku</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aberrant expression of interleukin-10 and activation-induced cytidine deaminase in B cells from patients with Behçet's disease</atitle><jtitle>Biomedical reports</jtitle><addtitle>Biomed Rep</addtitle><date>2017-12-01</date><risdate>2017</risdate><volume>7</volume><issue>6</issue><spage>520</spage><epage>526</epage><pages>520-526</pages><issn>2049-9434</issn><eissn>2049-9442</eissn><abstract>Despite extensive studies, the pathogenesis of Behçet's disease (BD) remains unclear. In particular, the roles of B cells in patients with BD have not been elucidated. Activation-induced cytidine deaminase (AID) is a critical enzyme for immunoglobulin (Ig) heavy chain class switching and somatic hypermutation in B cells and the abnormal expression of AID in various immune conditions has previously been studied. B10 cells, an interleukin (IL)-10-secreting subset of regulatory B cells, function to downregulate inflammation and autoimmunity. Thus, in the present study, the relevance of B cells in patients with BD was investigated. The plasma levels of IL-10 and IgA and the proportions of cluster of differentiation (CD)43+ B cells, excluding naïve B cells, were measured in 16 patients with BD and 16 age- and sex-matched healthy controls (HCs). Additionally, the mRNA levels of IL-10 and AID were assessed in B cells from fresh peripheral blood samples of the BD patients and HCs. The plasma level of IL-10 in patients with BD did not differ significantly from that in HCs. Similarly, there was no significant difference in the plasma level of IgA, although a slight increase was observed in patients with BD compared with that in HCs. There were no differences in CD43+CD19+ B cell numbers between patients with BD and HCs. However, IL-10 mRNA levels were significantly reduced (P<0.05), while AID mRNA levels were significantly increased (P<0.01) in the B cells of patients with BD compared with those in HCs. These results provide insight into the role of B cells in patients with BD.</abstract><cop>England</cop><pub>D.A. Spandidos</pub><pmid>29188055</pmid><doi>10.3892/br.2017.996</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aberration Activation-induced cytidine deaminase Autoimmunity B cells Behcet's syndrome Behçet's disease CD19 antigen CD43 antigen Cell activation Class switching cluster of differentiation 43 Cytidine deaminase Enzyme-linked immunosorbent assay Enzymes Fluorescein Immunoglobulin A Inflammation Interleukin 10 Interleukins Lupus Lymphocyte receptors Lymphocytes Lymphocytes B Medical research mRNA Pathogenesis Patients Peripheral blood Plasma levels RNA Somatic hypermutation Somatotropin Studies Systemic lupus erythematosus T cell receptors |
title | Aberrant expression of interleukin-10 and activation-induced cytidine deaminase in B cells from patients with Behçet's disease |
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