Impact of myelin-specific antigen presenting B cells on T cell activation in multiple sclerosis
Abstract The role of B cells in the pathogenesis of Multiple Sclerosis (MS) is incompletely understood. Here we define a possible role for B cells as myelin-specific antigen presenting cells (B-APCs) in MS. Peripheral blood B cells (PBBC) isolated from both MS patients and healthy controls (HC) were...
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| Veröffentlicht in: | Clinical immunology (Orlando, Fla.) Fla.), 2008-09, Vol.128 (3), p.382-391 |
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| creator | Harp, Christopher T Lovett-Racke, Amy E Racke, Michael K Frohman, Elliot M Monson, Nancy L |
| description | Abstract The role of B cells in the pathogenesis of Multiple Sclerosis (MS) is incompletely understood. Here we define a possible role for B cells as myelin-specific antigen presenting cells (B-APCs) in MS. Peripheral blood B cells (PBBC) isolated from both MS patients and healthy controls (HC) were activated in vitro with either CD40L/IL-4 or a Class B CpG oligodeoxynucleotide (CpG ODN)/IL-2. Both activation techniques induced PBBCs to upregulate CD80 and HLA-DR, rendering them more efficient APCs than resting B cells. Although the CD40L/IL-4 B-APCs were highly effective in eliciting CNS-antigen specific proliferation by autologous T cells, CpG ODN/IL-2 stimulated B cells were not. Furthermore, CD40L/IL-4 B-APC induced responses by autologous CD4+ T cells were susceptible to blocking with anti-HLA-DR antibody, suggesting that T cell responses were specific for antigen presentation by B-APC. CNS-antigen specific CD8+ T cell proliferation was also blocked by HLA-DR, suggesting that CD8+ proliferation is in part dependent on CD4+ help. |
| doi_str_mv | 10.1016/j.clim.2008.05.002 |
| format | Article |
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Here we define a possible role for B cells as myelin-specific antigen presenting cells (B-APCs) in MS. Peripheral blood B cells (PBBC) isolated from both MS patients and healthy controls (HC) were activated in vitro with either CD40L/IL-4 or a Class B CpG oligodeoxynucleotide (CpG ODN)/IL-2. Both activation techniques induced PBBCs to upregulate CD80 and HLA-DR, rendering them more efficient APCs than resting B cells. Although the CD40L/IL-4 B-APCs were highly effective in eliciting CNS-antigen specific proliferation by autologous T cells, CpG ODN/IL-2 stimulated B cells were not. Furthermore, CD40L/IL-4 B-APC induced responses by autologous CD4+ T cells were susceptible to blocking with anti-HLA-DR antibody, suggesting that T cell responses were specific for antigen presentation by B-APC. CNS-antigen specific CD8+ T cell proliferation was also blocked by HLA-DR, suggesting that CD8+ proliferation is in part dependent on CD4+ help.</description><identifier>ISSN: 1521-6616</identifier><identifier>ISSN: 0090-1229</identifier><identifier>EISSN: 1521-7035</identifier><identifier>DOI: 10.1016/j.clim.2008.05.002</identifier><identifier>PMID: 18599355</identifier><identifier>CODEN: CLIIFY</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>Allergy and Immunology ; Antigen presentation ; Antigen-Presenting Cells - immunology ; Autoimmunity ; B cells ; B-Lymphocyte Subsets - immunology ; B7-1 Antigen - immunology ; B7-1 Antigen - metabolism ; Biological and medical sciences ; CD4-Positive T-Lymphocytes - immunology ; CD40 Ligand - immunology ; CD8-Positive T-Lymphocytes - immunology ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; HLA-DR Antigens - immunology ; HLA-DR Antigens - metabolism ; Humans ; Interleukin-2 - immunology ; Interleukin-4 - immunology ; Lymphocyte Activation ; Medical sciences ; Multiple sclerosis ; Multiple Sclerosis - immunology ; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis ; Myelin Sheath - immunology ; Neurology ; Oligodeoxyribonucleotides - immunology ; Up-Regulation</subject><ispartof>Clinical immunology (Orlando, Fla.), 2008-09, Vol.128 (3), p.382-391</ispartof><rights>Elsevier Inc.</rights><rights>2008 Elsevier Inc.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-1a1606275826b72817a4a7d83fef848529cf744b0a10a02d51a2312d58dbd62a3</citedby><cites>FETCH-LOGICAL-c470t-1a1606275826b72817a4a7d83fef848529cf744b0a10a02d51a2312d58dbd62a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.clim.2008.05.002$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20618194$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18599355$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Harp, Christopher T</creatorcontrib><creatorcontrib>Lovett-Racke, Amy E</creatorcontrib><creatorcontrib>Racke, Michael K</creatorcontrib><creatorcontrib>Frohman, Elliot M</creatorcontrib><creatorcontrib>Monson, Nancy L</creatorcontrib><title>Impact of myelin-specific antigen presenting B cells on T cell activation in multiple sclerosis</title><title>Clinical immunology (Orlando, Fla.)</title><addtitle>Clin Immunol</addtitle><description>Abstract The role of B cells in the pathogenesis of Multiple Sclerosis (MS) is incompletely understood. Here we define a possible role for B cells as myelin-specific antigen presenting cells (B-APCs) in MS. Peripheral blood B cells (PBBC) isolated from both MS patients and healthy controls (HC) were activated in vitro with either CD40L/IL-4 or a Class B CpG oligodeoxynucleotide (CpG ODN)/IL-2. Both activation techniques induced PBBCs to upregulate CD80 and HLA-DR, rendering them more efficient APCs than resting B cells. Although the CD40L/IL-4 B-APCs were highly effective in eliciting CNS-antigen specific proliferation by autologous T cells, CpG ODN/IL-2 stimulated B cells were not. Furthermore, CD40L/IL-4 B-APC induced responses by autologous CD4+ T cells were susceptible to blocking with anti-HLA-DR antibody, suggesting that T cell responses were specific for antigen presentation by B-APC. CNS-antigen specific CD8+ T cell proliferation was also blocked by HLA-DR, suggesting that CD8+ proliferation is in part dependent on CD4+ help.</description><subject>Allergy and Immunology</subject><subject>Antigen presentation</subject><subject>Antigen-Presenting Cells - immunology</subject><subject>Autoimmunity</subject><subject>B cells</subject><subject>B-Lymphocyte Subsets - immunology</subject><subject>B7-1 Antigen - immunology</subject><subject>B7-1 Antigen - metabolism</subject><subject>Biological and medical sciences</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD40 Ligand - immunology</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>HLA-DR Antigens - immunology</subject><subject>HLA-DR Antigens - metabolism</subject><subject>Humans</subject><subject>Interleukin-2 - immunology</subject><subject>Interleukin-4 - immunology</subject><subject>Lymphocyte Activation</subject><subject>Medical sciences</subject><subject>Multiple sclerosis</subject><subject>Multiple Sclerosis - immunology</subject><subject>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</subject><subject>Myelin Sheath - immunology</subject><subject>Neurology</subject><subject>Oligodeoxyribonucleotides - immunology</subject><subject>Up-Regulation</subject><issn>1521-6616</issn><issn>0090-1229</issn><issn>1521-7035</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkk9v1DAQxS0EomXhC3BAvtBbwtiOHUdCSFDxp1KlHlrOlteZVF4SJ9hJpf32ddgIJA5wmpH1e-Pn5yHkNYOSAVPvDqXr_VByAF2CLAH4E3LOJGdFDUI-3XqlmDojL1I6AIDkXD0nZ0zLphFSnhNzNUzWzXTs6HDE3ociTeh85x21Yfb3GOgUMWHuwz39RB32faJjoHe_Wpq1_sHOPp_4QIeln_3UI02uxzgmn16SZ53tE77a6o58__L57vJbcX3z9ery43XhqhrmglmmQPFaaq72NdestpWtWy067HSlJW9cV1fVHiwDC7yVzHLBctXtvlXcih25OM2d4vhzwTSbwafVoQ04LsmophKilvV_QQ66YYLpDPIT6PJDUsTOTNEPNh4NA7Pmbw5mzd-s-RuQJuefRW-26ct-wPaPZAs8A283wCZn-y7a4Hz6zXFQTLPsdUfenzjMoT14jCY5j8Fh6yO62bSj_7ePD3_JMxJ8vvEHHjEdxiWG_B2GmcQNmNt1U9ZFAQ2gpADxCL3rt5I</recordid><startdate>20080901</startdate><enddate>20080901</enddate><creator>Harp, Christopher T</creator><creator>Lovett-Racke, Amy E</creator><creator>Racke, Michael K</creator><creator>Frohman, Elliot M</creator><creator>Monson, Nancy L</creator><general>Elsevier Inc</general><general>Elsevier</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20080901</creationdate><title>Impact of myelin-specific antigen presenting B cells on T cell activation in multiple sclerosis</title><author>Harp, Christopher T ; Lovett-Racke, Amy E ; Racke, Michael K ; Frohman, Elliot M ; Monson, Nancy L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-1a1606275826b72817a4a7d83fef848529cf744b0a10a02d51a2312d58dbd62a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Allergy and Immunology</topic><topic>Antigen presentation</topic><topic>Antigen-Presenting Cells - immunology</topic><topic>Autoimmunity</topic><topic>B cells</topic><topic>B-Lymphocyte Subsets - immunology</topic><topic>B7-1 Antigen - immunology</topic><topic>B7-1 Antigen - metabolism</topic><topic>Biological and medical sciences</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>CD40 Ligand - immunology</topic><topic>CD8-Positive T-Lymphocytes - immunology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>HLA-DR Antigens - immunology</topic><topic>HLA-DR Antigens - metabolism</topic><topic>Humans</topic><topic>Interleukin-2 - immunology</topic><topic>Interleukin-4 - immunology</topic><topic>Lymphocyte Activation</topic><topic>Medical sciences</topic><topic>Multiple sclerosis</topic><topic>Multiple Sclerosis - immunology</topic><topic>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</topic><topic>Myelin Sheath - immunology</topic><topic>Neurology</topic><topic>Oligodeoxyribonucleotides - immunology</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Harp, Christopher T</creatorcontrib><creatorcontrib>Lovett-Racke, Amy E</creatorcontrib><creatorcontrib>Racke, Michael K</creatorcontrib><creatorcontrib>Frohman, Elliot M</creatorcontrib><creatorcontrib>Monson, Nancy L</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical immunology (Orlando, Fla.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Harp, Christopher T</au><au>Lovett-Racke, Amy E</au><au>Racke, Michael K</au><au>Frohman, Elliot M</au><au>Monson, Nancy L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impact of myelin-specific antigen presenting B cells on T cell activation in multiple sclerosis</atitle><jtitle>Clinical immunology (Orlando, Fla.)</jtitle><addtitle>Clin Immunol</addtitle><date>2008-09-01</date><risdate>2008</risdate><volume>128</volume><issue>3</issue><spage>382</spage><epage>391</epage><pages>382-391</pages><issn>1521-6616</issn><issn>0090-1229</issn><eissn>1521-7035</eissn><coden>CLIIFY</coden><abstract>Abstract The role of B cells in the pathogenesis of Multiple Sclerosis (MS) is incompletely understood. Here we define a possible role for B cells as myelin-specific antigen presenting cells (B-APCs) in MS. Peripheral blood B cells (PBBC) isolated from both MS patients and healthy controls (HC) were activated in vitro with either CD40L/IL-4 or a Class B CpG oligodeoxynucleotide (CpG ODN)/IL-2. Both activation techniques induced PBBCs to upregulate CD80 and HLA-DR, rendering them more efficient APCs than resting B cells. Although the CD40L/IL-4 B-APCs were highly effective in eliciting CNS-antigen specific proliferation by autologous T cells, CpG ODN/IL-2 stimulated B cells were not. Furthermore, CD40L/IL-4 B-APC induced responses by autologous CD4+ T cells were susceptible to blocking with anti-HLA-DR antibody, suggesting that T cell responses were specific for antigen presentation by B-APC. 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| ispartof | Clinical immunology (Orlando, Fla.), 2008-09, Vol.128 (3), p.382-391 |
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| subjects | Allergy and Immunology Antigen presentation Antigen-Presenting Cells - immunology Autoimmunity B cells B-Lymphocyte Subsets - immunology B7-1 Antigen - immunology B7-1 Antigen - metabolism Biological and medical sciences CD4-Positive T-Lymphocytes - immunology CD40 Ligand - immunology CD8-Positive T-Lymphocytes - immunology Fundamental and applied biological sciences. Psychology Fundamental immunology HLA-DR Antigens - immunology HLA-DR Antigens - metabolism Humans Interleukin-2 - immunology Interleukin-4 - immunology Lymphocyte Activation Medical sciences Multiple sclerosis Multiple Sclerosis - immunology Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis Myelin Sheath - immunology Neurology Oligodeoxyribonucleotides - immunology Up-Regulation |
| title | Impact of myelin-specific antigen presenting B cells on T cell activation in multiple sclerosis |
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