B-cell receptor cross-linking delays activation-induced cytidine deaminase induction and inhibits class-switch recombination to IgE
Background During differentiation, B cells receive signals by antigen through the B-cell receptor (BCR) and signals that induce isotype switching. Objective We sought to investigate the effects of BCR ligation on isotype switching. Methods Naive B cells from BALB/c mice were stimulated with LPS plus...
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| creator | Jabara, Haifa H., BS Chaudhuri, Jayanta, PhD Dutt, Shilpee, PhD Dedeoglu, Fatma, MD Weng, Yu, BS Murphy, Michael M., BS Franco, Sonia, MD, PhD Alt, Fredrick W., PhD Manis, John, MD Geha, Raif S., MD |
| description | Background During differentiation, B cells receive signals by antigen through the B-cell receptor (BCR) and signals that induce isotype switching. Objective We sought to investigate the effects of BCR ligation on isotype switching. Methods Naive B cells from BALB/c mice were stimulated with LPS plus IL-4 alone or plus anti-IgM (0.1-10 μg/mL). IgE and IgG1 levels in supernatants were measured by means of ELISA on day 6. Cμ or Cε germline transcripts, activation-induced cytidine deaminase (AID), and Iμ-Cε postswitch transcripts were measured by means of RT-PCR. Deletional switch recombination was assessed by means of digestion circularization PCR of Sμ-Sε products. Results BCR cross-linking inhibited IgE and IgG1 switching in a dose-dependent fashion. This was not due to inhibition of proliferation, increased apoptosis, or cell death. BCR cross-linking had no effect on Cμ or Cε germline transcripts but suppressed the generation of Sμ-Sε switch products and Iμ-Cε postswitch transcripts and caused a delay in the expression of AID mRNA, with decreased expression on days 2 and 3 after stimulation. Concomitantly, the number of DNA repair foci at the IgH locus on day 3 was significantly decreased. AID expression and activity became normal on day 4, but isotype switching remained profoundly diminished 8 days after stimulation. Conclusion BCR cross-linking delays AID expression. This might interfere with class-switch recombination by disrupting the temporal coordination of signals that lead to class-switch recombination. |
| doi_str_mv | 10.1016/j.jaci.2007.08.008 |
| format | Article |
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Objective We sought to investigate the effects of BCR ligation on isotype switching. Methods Naive B cells from BALB/c mice were stimulated with LPS plus IL-4 alone or plus anti-IgM (0.1-10 μg/mL). IgE and IgG1 levels in supernatants were measured by means of ELISA on day 6. Cμ or Cε germline transcripts, activation-induced cytidine deaminase (AID), and Iμ-Cε postswitch transcripts were measured by means of RT-PCR. Deletional switch recombination was assessed by means of digestion circularization PCR of Sμ-Sε products. Results BCR cross-linking inhibited IgE and IgG1 switching in a dose-dependent fashion. This was not due to inhibition of proliferation, increased apoptosis, or cell death. BCR cross-linking had no effect on Cμ or Cε germline transcripts but suppressed the generation of Sμ-Sε switch products and Iμ-Cε postswitch transcripts and caused a delay in the expression of AID mRNA, with decreased expression on days 2 and 3 after stimulation. Concomitantly, the number of DNA repair foci at the IgH locus on day 3 was significantly decreased. AID expression and activity became normal on day 4, but isotype switching remained profoundly diminished 8 days after stimulation. Conclusion BCR cross-linking delays AID expression. This might interfere with class-switch recombination by disrupting the temporal coordination of signals that lead to class-switch recombination.</description><identifier>ISSN: 0091-6749</identifier><identifier>EISSN: 1097-6825</identifier><identifier>DOI: 10.1016/j.jaci.2007.08.008</identifier><identifier>PMID: 17900678</identifier><identifier>CODEN: JACIBY</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>activation-induced cytidine deaminase ; Allergy and Immunology ; Animals ; B-cell receptor ; B-Lymphocytes - metabolism ; Biological and medical sciences ; Cells, Cultured ; Cytidine Deaminase - biosynthesis ; Enzyme Induction ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; IgE ; Immune system ; Immunoglobulin Class Switching - genetics ; Immunoglobulin Class Switching - immunology ; Immunoglobulin E - biosynthesis ; Immunoglobulin G - biosynthesis ; Immunoglobulins ; Immunopathology ; isotype switching ; Kinases ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Receptors, Antigen, B-Cell - metabolism ; Recombination, Genetic ; Rodents ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</subject><ispartof>Journal of allergy and clinical immunology, 2008, Vol.121 (1), p.191-196.e2</ispartof><rights>American Academy of Allergy, Asthma & Immunology</rights><rights>2008 American Academy of Allergy, Asthma & Immunology</rights><rights>2008 INIST-CNRS</rights><rights>Copyright Elsevier Limited Jan 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c560t-cd199b19650bd97788c69d08ff7b7bc81d35b8e1a16a4a96c879630dfd5b9be83</citedby><cites>FETCH-LOGICAL-c560t-cd199b19650bd97788c69d08ff7b7bc81d35b8e1a16a4a96c879630dfd5b9be83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jaci.2007.08.008$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,4024,27923,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20369664$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17900678$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jabara, Haifa H., BS</creatorcontrib><creatorcontrib>Chaudhuri, Jayanta, PhD</creatorcontrib><creatorcontrib>Dutt, Shilpee, PhD</creatorcontrib><creatorcontrib>Dedeoglu, Fatma, MD</creatorcontrib><creatorcontrib>Weng, Yu, BS</creatorcontrib><creatorcontrib>Murphy, Michael M., BS</creatorcontrib><creatorcontrib>Franco, Sonia, MD, PhD</creatorcontrib><creatorcontrib>Alt, Fredrick W., PhD</creatorcontrib><creatorcontrib>Manis, John, MD</creatorcontrib><creatorcontrib>Geha, Raif S., MD</creatorcontrib><title>B-cell receptor cross-linking delays activation-induced cytidine deaminase induction and inhibits class-switch recombination to IgE</title><title>Journal of allergy and clinical immunology</title><addtitle>J Allergy Clin Immunol</addtitle><description>Background During differentiation, B cells receive signals by antigen through the B-cell receptor (BCR) and signals that induce isotype switching. Objective We sought to investigate the effects of BCR ligation on isotype switching. Methods Naive B cells from BALB/c mice were stimulated with LPS plus IL-4 alone or plus anti-IgM (0.1-10 μg/mL). IgE and IgG1 levels in supernatants were measured by means of ELISA on day 6. Cμ or Cε germline transcripts, activation-induced cytidine deaminase (AID), and Iμ-Cε postswitch transcripts were measured by means of RT-PCR. Deletional switch recombination was assessed by means of digestion circularization PCR of Sμ-Sε products. Results BCR cross-linking inhibited IgE and IgG1 switching in a dose-dependent fashion. This was not due to inhibition of proliferation, increased apoptosis, or cell death. BCR cross-linking had no effect on Cμ or Cε germline transcripts but suppressed the generation of Sμ-Sε switch products and Iμ-Cε postswitch transcripts and caused a delay in the expression of AID mRNA, with decreased expression on days 2 and 3 after stimulation. Concomitantly, the number of DNA repair foci at the IgH locus on day 3 was significantly decreased. AID expression and activity became normal on day 4, but isotype switching remained profoundly diminished 8 days after stimulation. Conclusion BCR cross-linking delays AID expression. This might interfere with class-switch recombination by disrupting the temporal coordination of signals that lead to class-switch recombination.</description><subject>activation-induced cytidine deaminase</subject><subject>Allergy and Immunology</subject><subject>Animals</subject><subject>B-cell receptor</subject><subject>B-Lymphocytes - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cells, Cultured</subject><subject>Cytidine Deaminase - biosynthesis</subject><subject>Enzyme Induction</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>IgE</subject><subject>Immune system</subject><subject>Immunoglobulin Class Switching - genetics</subject><subject>Immunoglobulin Class Switching - immunology</subject><subject>Immunoglobulin E - biosynthesis</subject><subject>Immunoglobulin G - biosynthesis</subject><subject>Immunoglobulins</subject><subject>Immunopathology</subject><subject>isotype switching</subject><subject>Kinases</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Receptors, Antigen, B-Cell - metabolism</subject><subject>Recombination, Genetic</subject><subject>Rodents</subject><subject>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</subject><issn>0091-6749</issn><issn>1097-6825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkktv1DAQgC0EokvhD3BAkRC9JYyT-CWhSlAVqFSJA3C2_ErrNOssdlK05_5xnN0VlXqAnqyRvxnPeD6EXmOoMGD6vq96ZXxVA7AKeAXAn6AVBsFKymvyFK0ABC4pa8URepFSDzluuHiOjjATAJTxFbr7VBo3DEV0xm2mMRYmjimVgw83PlwV1g1qmwplJn-rJj-G0gc7G2cLs5289cFlRK19UMkVu6sFKlSwObr22k-pMIPKFdNvP5nr5Z1xrTO_46axuLg6f4medWpI7tXhPEY_P5__OPtaXn77cnH28bI0hMJUGouF0FhQAtoKxjg3VFjgXcc004Zj2xDNHVaYqlYJajgTtAHbWaKFdrw5Rif7ups4_ppdmuTap2V6Fdw4J8mgxkQQ8V8QCw6tAPIIMLeAcfMIkDScQ53Btw_AfpxjyN8iMYGWMYZhmaTeU7ttRdfJTfRrFbcSg1zckL1c3JCLGxK4hF3Sm0PpWa-dvU85yJCBdwdAJaOGLqpgfPrL1dBQQWmbuQ97zuVl3XoXZTLehWyFz-udpB39v_s4fZBusm4-v3jjti7dzytTLUF-XyxeJAYGmDQ1bv4AkZ3tZA</recordid><startdate>2008</startdate><enddate>2008</enddate><creator>Jabara, Haifa H., BS</creator><creator>Chaudhuri, Jayanta, PhD</creator><creator>Dutt, Shilpee, PhD</creator><creator>Dedeoglu, Fatma, MD</creator><creator>Weng, Yu, BS</creator><creator>Murphy, Michael M., BS</creator><creator>Franco, Sonia, MD, PhD</creator><creator>Alt, Fredrick W., PhD</creator><creator>Manis, John, MD</creator><creator>Geha, Raif S., MD</creator><general>Mosby, Inc</general><general>Elsevier</general><general>Elsevier Limited</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>7SS</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7TM</scope><scope>7X8</scope></search><sort><creationdate>2008</creationdate><title>B-cell receptor cross-linking delays activation-induced cytidine deaminase induction and inhibits class-switch recombination to IgE</title><author>Jabara, Haifa H., BS ; Chaudhuri, Jayanta, PhD ; Dutt, Shilpee, PhD ; Dedeoglu, Fatma, MD ; Weng, Yu, BS ; Murphy, Michael M., BS ; Franco, Sonia, MD, PhD ; Alt, Fredrick W., PhD ; Manis, John, MD ; Geha, Raif S., MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c560t-cd199b19650bd97788c69d08ff7b7bc81d35b8e1a16a4a96c879630dfd5b9be83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>activation-induced cytidine deaminase</topic><topic>Allergy and Immunology</topic><topic>Animals</topic><topic>B-cell receptor</topic><topic>B-Lymphocytes - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cells, Cultured</topic><topic>Cytidine Deaminase - biosynthesis</topic><topic>Enzyme Induction</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>IgE</topic><topic>Immune system</topic><topic>Immunoglobulin Class Switching - genetics</topic><topic>Immunoglobulin Class Switching - immunology</topic><topic>Immunoglobulin E - biosynthesis</topic><topic>Immunoglobulin G - biosynthesis</topic><topic>Immunoglobulins</topic><topic>Immunopathology</topic><topic>isotype switching</topic><topic>Kinases</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Receptors, Antigen, B-Cell - metabolism</topic><topic>Recombination, Genetic</topic><topic>Rodents</topic><topic>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jabara, Haifa H., BS</creatorcontrib><creatorcontrib>Chaudhuri, Jayanta, PhD</creatorcontrib><creatorcontrib>Dutt, Shilpee, PhD</creatorcontrib><creatorcontrib>Dedeoglu, Fatma, MD</creatorcontrib><creatorcontrib>Weng, Yu, BS</creatorcontrib><creatorcontrib>Murphy, Michael M., BS</creatorcontrib><creatorcontrib>Franco, Sonia, MD, PhD</creatorcontrib><creatorcontrib>Alt, Fredrick W., PhD</creatorcontrib><creatorcontrib>Manis, John, MD</creatorcontrib><creatorcontrib>Geha, Raif S., MD</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>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of allergy and clinical immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jabara, Haifa H., BS</au><au>Chaudhuri, Jayanta, PhD</au><au>Dutt, Shilpee, PhD</au><au>Dedeoglu, Fatma, MD</au><au>Weng, Yu, BS</au><au>Murphy, Michael M., BS</au><au>Franco, Sonia, MD, PhD</au><au>Alt, Fredrick W., PhD</au><au>Manis, John, MD</au><au>Geha, Raif S., MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>B-cell receptor cross-linking delays activation-induced cytidine deaminase induction and inhibits class-switch recombination to IgE</atitle><jtitle>Journal of allergy and clinical immunology</jtitle><addtitle>J Allergy Clin Immunol</addtitle><date>2008</date><risdate>2008</risdate><volume>121</volume><issue>1</issue><spage>191</spage><epage>196.e2</epage><pages>191-196.e2</pages><issn>0091-6749</issn><eissn>1097-6825</eissn><coden>JACIBY</coden><abstract>Background During differentiation, B cells receive signals by antigen through the B-cell receptor (BCR) and signals that induce isotype switching. Objective We sought to investigate the effects of BCR ligation on isotype switching. Methods Naive B cells from BALB/c mice were stimulated with LPS plus IL-4 alone or plus anti-IgM (0.1-10 μg/mL). IgE and IgG1 levels in supernatants were measured by means of ELISA on day 6. Cμ or Cε germline transcripts, activation-induced cytidine deaminase (AID), and Iμ-Cε postswitch transcripts were measured by means of RT-PCR. Deletional switch recombination was assessed by means of digestion circularization PCR of Sμ-Sε products. Results BCR cross-linking inhibited IgE and IgG1 switching in a dose-dependent fashion. This was not due to inhibition of proliferation, increased apoptosis, or cell death. BCR cross-linking had no effect on Cμ or Cε germline transcripts but suppressed the generation of Sμ-Sε switch products and Iμ-Cε postswitch transcripts and caused a delay in the expression of AID mRNA, with decreased expression on days 2 and 3 after stimulation. Concomitantly, the number of DNA repair foci at the IgH locus on day 3 was significantly decreased. AID expression and activity became normal on day 4, but isotype switching remained profoundly diminished 8 days after stimulation. Conclusion BCR cross-linking delays AID expression. This might interfere with class-switch recombination by disrupting the temporal coordination of signals that lead to class-switch recombination.</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>17900678</pmid><doi>10.1016/j.jaci.2007.08.008</doi><tpages>6</tpages></addata></record> |
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| subjects | activation-induced cytidine deaminase Allergy and Immunology Animals B-cell receptor B-Lymphocytes - metabolism Biological and medical sciences Cells, Cultured Cytidine Deaminase - biosynthesis Enzyme Induction Fundamental and applied biological sciences. Psychology Fundamental immunology IgE Immune system Immunoglobulin Class Switching - genetics Immunoglobulin Class Switching - immunology Immunoglobulin E - biosynthesis Immunoglobulin G - biosynthesis Immunoglobulins Immunopathology isotype switching Kinases Medical sciences Mice Mice, Inbred BALB C Receptors, Antigen, B-Cell - metabolism Recombination, Genetic Rodents Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis |
| title | B-cell receptor cross-linking delays activation-induced cytidine deaminase induction and inhibits class-switch recombination to IgE |
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