Actions of BAFF in B cell maturation and its effects on the development of autoimmune disease
BAFF, a member of the family of tumour necrosis factor (TNF) ligands, is essential for the development of peripheral mature, long lived B lymphocytes. It binds to three different receptors, BCMA, TACI, and BAFF-R, which are all members of the family of TNF receptors. Defects in the genes encoding BA...
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| Veröffentlicht in: | Annals of the rheumatic diseases 2003-11, Vol.62 (suppl 2), p.ii25-ii27 |
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| description | BAFF, a member of the family of tumour necrosis factor (TNF) ligands, is essential for the development of peripheral mature, long lived B lymphocytes. It binds to three different receptors, BCMA, TACI, and BAFF-R, which are all members of the family of TNF receptors. Defects in the genes encoding BAFF or BAFF-R abolish the generation of mature B cells. BAFF is made by myeloid cells whereas BAFF-R is expressed preferentially on B cells. BAFF induces polyclonal maturation of resting, short lived immature B cells to resting, long lived mature B cells without proliferation. Lupus erythematodes prone mice have elevated blood levels of BAFF, and treatment of these mice with the BAFF decoy receptor (BCMA-Ig) prevents the onset of this systemic autoimmune disease. Human lupus patients also have elevated blood levels of BAFF. Treatment with BAFF neutralising agents (decoy receptors, monoclonal antibodies) should prevent, delay, or, at least, slow down the disease. |
| doi_str_mv | 10.1136/ard.62.suppl_2.ii25 |
| format | Article |
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It binds to three different receptors, BCMA, TACI, and BAFF-R, which are all members of the family of TNF receptors. Defects in the genes encoding BAFF or BAFF-R abolish the generation of mature B cells. BAFF is made by myeloid cells whereas BAFF-R is expressed preferentially on B cells. BAFF induces polyclonal maturation of resting, short lived immature B cells to resting, long lived mature B cells without proliferation. Lupus erythematodes prone mice have elevated blood levels of BAFF, and treatment of these mice with the BAFF decoy receptor (BCMA-Ig) prevents the onset of this systemic autoimmune disease. Human lupus patients also have elevated blood levels of BAFF. Treatment with BAFF neutralising agents (decoy receptors, monoclonal antibodies) should prevent, delay, or, at least, slow down the disease.</description><identifier>ISSN: 0003-4967</identifier><identifier>EISSN: 1468-2060</identifier><identifier>DOI: 10.1136/ard.62.suppl_2.ii25</identifier><identifier>PMID: 14532143</identifier><identifier>CODEN: ARDIAO</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and European League Against Rheumatism</publisher><subject>Animals ; Antigens ; Apoptosis ; autoimmune disease ; Autoimmune diseases ; Autoimmune Diseases - immunology ; B cell maturation ; B-Cell Activating Factor ; B-Cell Activation Factor Receptor ; B-Lymphocytes - immunology ; BAFF ; Biological and medical sciences ; Bone marrow ; Cell Differentiation - immunology ; Ligands ; Lupus ; Lupus Erythematosus, Systemic - immunology ; Lymphocyte receptors ; Lymphocytes ; Medical sciences ; Membrane Proteins - immunology ; Mice ; Mice, Transgenic ; Receptors, Tumor Necrosis Factor - immunology ; Rodents ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; Tumor Necrosis Factor-alpha - immunology ; Tumor necrosis factor-TNF</subject><ispartof>Annals of the rheumatic diseases, 2003-11, Vol.62 (suppl 2), p.ii25-ii27</ispartof><rights>Copyright 2003 by Annals of the Rheumatic Diseases</rights><rights>2004 INIST-CNRS</rights><rights>Copyright: 2003 Copyright 2003 by Annals of the Rheumatic Diseases</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b536t-d8a318e998608c8a43fe14b4ec7e91c1151d80bb98bf2fa9a365eafd15b3d27e3</citedby><cites>FETCH-LOGICAL-b536t-d8a318e998608c8a43fe14b4ec7e91c1151d80bb98bf2fa9a365eafd15b3d27e3</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/PMC1766741/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1766741/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,309,310,314,727,780,784,789,790,885,23929,23930,25139,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15234933$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14532143$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Melchers, F</creatorcontrib><title>Actions of BAFF in B cell maturation and its effects on the development of autoimmune disease</title><title>Annals of the rheumatic diseases</title><addtitle>Ann Rheum Dis</addtitle><description>BAFF, a member of the family of tumour necrosis factor (TNF) ligands, is essential for the development of peripheral mature, long lived B lymphocytes. It binds to three different receptors, BCMA, TACI, and BAFF-R, which are all members of the family of TNF receptors. Defects in the genes encoding BAFF or BAFF-R abolish the generation of mature B cells. BAFF is made by myeloid cells whereas BAFF-R is expressed preferentially on B cells. BAFF induces polyclonal maturation of resting, short lived immature B cells to resting, long lived mature B cells without proliferation. Lupus erythematodes prone mice have elevated blood levels of BAFF, and treatment of these mice with the BAFF decoy receptor (BCMA-Ig) prevents the onset of this systemic autoimmune disease. Human lupus patients also have elevated blood levels of BAFF. Treatment with BAFF neutralising agents (decoy receptors, monoclonal antibodies) should prevent, delay, or, at least, slow down the disease.</description><subject>Animals</subject><subject>Antigens</subject><subject>Apoptosis</subject><subject>autoimmune disease</subject><subject>Autoimmune diseases</subject><subject>Autoimmune Diseases - immunology</subject><subject>B cell maturation</subject><subject>B-Cell Activating Factor</subject><subject>B-Cell Activation Factor Receptor</subject><subject>B-Lymphocytes - immunology</subject><subject>BAFF</subject><subject>Biological and medical sciences</subject><subject>Bone marrow</subject><subject>Cell Differentiation - immunology</subject><subject>Ligands</subject><subject>Lupus</subject><subject>Lupus Erythematosus, Systemic - immunology</subject><subject>Lymphocyte receptors</subject><subject>Lymphocytes</subject><subject>Medical sciences</subject><subject>Membrane Proteins - immunology</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Receptors, Tumor Necrosis Factor - immunology</subject><subject>Rodents</subject><subject>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</subject><subject>Tumor Necrosis Factor-alpha - immunology</subject><subject>Tumor necrosis factor-TNF</subject><issn>0003-4967</issn><issn>1468-2060</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkVuLFDEQhYMo7rj6CwRpEH3rNulc-0WYGRwvjPqyXhAkpNMVN2PfTLoX_femmWFXffKpSM5Xh6o6CD0kuCCEimcmNIUoiziPY6vLwvuS30IrwoTKSyzwbbTCGNOcVUKeoXsxHtITK6LuojPCOC0Joyv0dW0nP_QxG1y2We92me-zTWahbbPOTHMwi5qZvsn8FDNwDmyq6Wu6hKyBK2iHsYN-WvrNPA2-6-Y-KT6CiXAf3XGmjfDgVM_Rh92Li-2rfP_-5evtep_XnIopb5ShREFVKYGVVYZRB4TVDKyEilhCOGkUrutK1a50pjJUcDCuIbymTSmBnqPnR99xrjtobBoomFaPwXcm_NKD8fpvpfeX-ttwpYkUQjKSDJ6eDMLwY4Y46c7H5Qqmh2GOWnIpMOYqgY__AQ_DHPq0XPKSslKsFCJR9EjZMMQYwF2PQrBewtMpPC1KfQpPL-Glrkd_bnHTc0orAU9OgInWtC6Y3vp4w_GSsoouXH7kfJzg57VuwnctJJVcv_u41W_o5u2niy-f9T7xxZGvu8N_Tfob0wHF6w</recordid><startdate>20031101</startdate><enddate>20031101</enddate><creator>Melchers, F</creator><general>BMJ Publishing Group Ltd and European League Against Rheumatism</general><general>BMJ</general><general>Elsevier Limited</general><scope>BSCLL</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20031101</creationdate><title>Actions of BAFF in B cell maturation and its effects on the development of autoimmune disease</title><author>Melchers, F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b536t-d8a318e998608c8a43fe14b4ec7e91c1151d80bb98bf2fa9a365eafd15b3d27e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Antigens</topic><topic>Apoptosis</topic><topic>autoimmune disease</topic><topic>Autoimmune diseases</topic><topic>Autoimmune Diseases - immunology</topic><topic>B cell maturation</topic><topic>B-Cell Activating Factor</topic><topic>B-Cell Activation Factor Receptor</topic><topic>B-Lymphocytes - immunology</topic><topic>BAFF</topic><topic>Biological and medical sciences</topic><topic>Bone marrow</topic><topic>Cell Differentiation - immunology</topic><topic>Ligands</topic><topic>Lupus</topic><topic>Lupus Erythematosus, Systemic - immunology</topic><topic>Lymphocyte receptors</topic><topic>Lymphocytes</topic><topic>Medical sciences</topic><topic>Membrane Proteins - immunology</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Receptors, Tumor Necrosis Factor - immunology</topic><topic>Rodents</topic><topic>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</topic><topic>Tumor Necrosis Factor-alpha - immunology</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Melchers, F</creatorcontrib><collection>Istex</collection><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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Annals of the rheumatic diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Melchers, F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Actions of BAFF in B cell maturation and its effects on the development of autoimmune disease</atitle><jtitle>Annals of the rheumatic diseases</jtitle><addtitle>Ann Rheum Dis</addtitle><date>2003-11-01</date><risdate>2003</risdate><volume>62</volume><issue>suppl 2</issue><spage>ii25</spage><epage>ii27</epage><pages>ii25-ii27</pages><issn>0003-4967</issn><eissn>1468-2060</eissn><coden>ARDIAO</coden><abstract>BAFF, a member of the family of tumour necrosis factor (TNF) ligands, is essential for the development of peripheral mature, long lived B lymphocytes. It binds to three different receptors, BCMA, TACI, and BAFF-R, which are all members of the family of TNF receptors. Defects in the genes encoding BAFF or BAFF-R abolish the generation of mature B cells. BAFF is made by myeloid cells whereas BAFF-R is expressed preferentially on B cells. BAFF induces polyclonal maturation of resting, short lived immature B cells to resting, long lived mature B cells without proliferation. Lupus erythematodes prone mice have elevated blood levels of BAFF, and treatment of these mice with the BAFF decoy receptor (BCMA-Ig) prevents the onset of this systemic autoimmune disease. Human lupus patients also have elevated blood levels of BAFF. Treatment with BAFF neutralising agents (decoy receptors, monoclonal antibodies) should prevent, delay, or, at least, slow down the disease.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and European League Against Rheumatism</pub><pmid>14532143</pmid><doi>10.1136/ard.62.suppl_2.ii25</doi><oa>free_for_read</oa></addata></record> |
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| ispartof | Annals of the rheumatic diseases, 2003-11, Vol.62 (suppl 2), p.ii25-ii27 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Animals Antigens Apoptosis autoimmune disease Autoimmune diseases Autoimmune Diseases - immunology B cell maturation B-Cell Activating Factor B-Cell Activation Factor Receptor B-Lymphocytes - immunology BAFF Biological and medical sciences Bone marrow Cell Differentiation - immunology Ligands Lupus Lupus Erythematosus, Systemic - immunology Lymphocyte receptors Lymphocytes Medical sciences Membrane Proteins - immunology Mice Mice, Transgenic Receptors, Tumor Necrosis Factor - immunology Rodents Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Tumor Necrosis Factor-alpha - immunology Tumor necrosis factor-TNF |
| title | Actions of BAFF in B cell maturation and its effects on the development of autoimmune disease |
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