A BAFF antagonist suppresses experimental autoimmune encephalomyelitis by targeting cell-mediated and humoral immune responses
BAFF [B cell-activating factor of the tumour necrosis factor (TNF) family] and APRIL (a proliferation-inducing ligand) are two TNF family members with shared receptors. While, physiological roles for APRIL are not fully understood, BAFF is critical for B cell homeostasis and also acts as a co-stimul...
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creator | Huntington, Nicholas D. Tomioka, Ryo Clavarino, Chelsea Chow, Anne M. Liñares, David Maña, Paula Rossjohn, Jamie Cachero, Teresa G. Qian, Fang Kalled, Susan L. Bernard, Claude C. A. Reid, Hugh H. |
description | BAFF [B cell-activating factor of the tumour necrosis factor (TNF) family] and APRIL (a proliferation-inducing ligand) are two TNF family members with shared receptors. While, physiological roles for APRIL are not fully understood, BAFF is critical for B cell homeostasis and also acts as a co-stimulator of T cells. Using a B and T cell-mediated mouse model of multiple sclerosis (MS), myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), we observed that a BAFF/APRIL antagonist (soluble BCMA-Fc) inhibited central nervous system inflammation and demyelination such that it suppressed the onset and progression of clinical symptoms of EAE. In addition to dramatically reducing the titre of MOG-specific auto-antibodies, this treatment also induced a switch in the subtype of the Th cell population characterized by marked alterations in cytokine production following re-stimulation with MOG in vitro. Indeed, hBCMA-Fc therapy led to significant increases in the level of transforming growth factor β, while the levels of Th1 cytokines were markedly diminished. These results not only identify BAFF as a critical factor in maintaining humoral immunity in EAE but also support its role in T lymphocyte responses. Our findings demonstrate that hBCMA-Fc acts on both effector arms of the immune response in EAE, a characteristic that may be of significant therapeutic value in the treatment of MS. |
doi_str_mv | 10.1093/intimm/dxl080 |
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A. ; Reid, Hugh H.</creator><creatorcontrib>Huntington, Nicholas D. ; Tomioka, Ryo ; Clavarino, Chelsea ; Chow, Anne M. ; Liñares, David ; Maña, Paula ; Rossjohn, Jamie ; Cachero, Teresa G. ; Qian, Fang ; Kalled, Susan L. ; Bernard, Claude C. A. ; Reid, Hugh H.</creatorcontrib><description>BAFF [B cell-activating factor of the tumour necrosis factor (TNF) family] and APRIL (a proliferation-inducing ligand) are two TNF family members with shared receptors. While, physiological roles for APRIL are not fully understood, BAFF is critical for B cell homeostasis and also acts as a co-stimulator of T cells. Using a B and T cell-mediated mouse model of multiple sclerosis (MS), myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), we observed that a BAFF/APRIL antagonist (soluble BCMA-Fc) inhibited central nervous system inflammation and demyelination such that it suppressed the onset and progression of clinical symptoms of EAE. In addition to dramatically reducing the titre of MOG-specific auto-antibodies, this treatment also induced a switch in the subtype of the Th cell population characterized by marked alterations in cytokine production following re-stimulation with MOG in vitro. Indeed, hBCMA-Fc therapy led to significant increases in the level of transforming growth factor β, while the levels of Th1 cytokines were markedly diminished. These results not only identify BAFF as a critical factor in maintaining humoral immunity in EAE but also support its role in T lymphocyte responses. Our findings demonstrate that hBCMA-Fc acts on both effector arms of the immune response in EAE, a characteristic that may be of significant therapeutic value in the treatment of MS.</description><identifier>ISSN: 0953-8178</identifier><identifier>EISSN: 1460-2377</identifier><identifier>DOI: 10.1093/intimm/dxl080</identifier><identifier>PMID: 16914508</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject><![CDATA[Animals ; Antibody Formation - drug effects ; Antibody Formation - immunology ; autoimmunity ; B-Cell Activating Factor - antagonists & inhibitors ; B-Cell Activating Factor - immunology ; B-Cell Maturation Antigen - administration & dosage ; B-Lymphocytes - immunology ; central nervous system diseases ; cytokine receptors ; cytokines ; Encephalomyelitis, Autoimmune, Experimental - chemically induced ; Encephalomyelitis, Autoimmune, Experimental - drug therapy ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Female ; Immunity, Cellular - drug effects ; Immunity, Cellular - immunology ; Immunoglobulin Fc Fragments - administration & dosage ; Mice ; Mice, Inbred NOD ; multiple sclerosis ; Multiple Sclerosis - chemically induced ; Multiple Sclerosis - drug therapy ; Multiple Sclerosis - immunology ; Myelin Proteins ; Myelin-Associated Glycoprotein - administration & dosage ; Myelin-Associated Glycoprotein - toxicity ; Myelin-Oligodendrocyte Glycoprotein ; Recombinant Fusion Proteins - administration & dosage ; T-Lymphocytes - immunology ; therapeutics ; Tumor Necrosis Factor Ligand Superfamily Member 13 - antagonists & inhibitors ; Tumor Necrosis Factor Ligand Superfamily Member 13 - immunology]]></subject><ispartof>International immunology, 2006-10, Vol.18 (10), p.1473-1485</ispartof><rights>Copyright Oxford University Press(England) Oct 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16914508$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huntington, Nicholas D.</creatorcontrib><creatorcontrib>Tomioka, Ryo</creatorcontrib><creatorcontrib>Clavarino, Chelsea</creatorcontrib><creatorcontrib>Chow, Anne M.</creatorcontrib><creatorcontrib>Liñares, David</creatorcontrib><creatorcontrib>Maña, Paula</creatorcontrib><creatorcontrib>Rossjohn, Jamie</creatorcontrib><creatorcontrib>Cachero, Teresa G.</creatorcontrib><creatorcontrib>Qian, Fang</creatorcontrib><creatorcontrib>Kalled, Susan L.</creatorcontrib><creatorcontrib>Bernard, Claude C. A.</creatorcontrib><creatorcontrib>Reid, Hugh H.</creatorcontrib><title>A BAFF antagonist suppresses experimental autoimmune encephalomyelitis by targeting cell-mediated and humoral immune responses</title><title>International immunology</title><addtitle>Int Immunol</addtitle><description>BAFF [B cell-activating factor of the tumour necrosis factor (TNF) family] and APRIL (a proliferation-inducing ligand) are two TNF family members with shared receptors. While, physiological roles for APRIL are not fully understood, BAFF is critical for B cell homeostasis and also acts as a co-stimulator of T cells. Using a B and T cell-mediated mouse model of multiple sclerosis (MS), myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), we observed that a BAFF/APRIL antagonist (soluble BCMA-Fc) inhibited central nervous system inflammation and demyelination such that it suppressed the onset and progression of clinical symptoms of EAE. In addition to dramatically reducing the titre of MOG-specific auto-antibodies, this treatment also induced a switch in the subtype of the Th cell population characterized by marked alterations in cytokine production following re-stimulation with MOG in vitro. Indeed, hBCMA-Fc therapy led to significant increases in the level of transforming growth factor β, while the levels of Th1 cytokines were markedly diminished. These results not only identify BAFF as a critical factor in maintaining humoral immunity in EAE but also support its role in T lymphocyte responses. Our findings demonstrate that hBCMA-Fc acts on both effector arms of the immune response in EAE, a characteristic that may be of significant therapeutic value in the treatment of MS.</description><subject>Animals</subject><subject>Antibody Formation - drug effects</subject><subject>Antibody Formation - immunology</subject><subject>autoimmunity</subject><subject>B-Cell Activating Factor - antagonists & inhibitors</subject><subject>B-Cell Activating Factor - immunology</subject><subject>B-Cell Maturation Antigen - administration & dosage</subject><subject>B-Lymphocytes - immunology</subject><subject>central nervous system diseases</subject><subject>cytokine receptors</subject><subject>cytokines</subject><subject>Encephalomyelitis, Autoimmune, Experimental - chemically induced</subject><subject>Encephalomyelitis, Autoimmune, Experimental - drug therapy</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Female</subject><subject>Immunity, Cellular - drug effects</subject><subject>Immunity, Cellular - immunology</subject><subject>Immunoglobulin Fc Fragments - administration & dosage</subject><subject>Mice</subject><subject>Mice, Inbred NOD</subject><subject>multiple sclerosis</subject><subject>Multiple Sclerosis - chemically induced</subject><subject>Multiple Sclerosis - drug therapy</subject><subject>Multiple Sclerosis - immunology</subject><subject>Myelin Proteins</subject><subject>Myelin-Associated Glycoprotein - administration & dosage</subject><subject>Myelin-Associated Glycoprotein - toxicity</subject><subject>Myelin-Oligodendrocyte Glycoprotein</subject><subject>Recombinant Fusion Proteins - administration & dosage</subject><subject>T-Lymphocytes - immunology</subject><subject>therapeutics</subject><subject>Tumor Necrosis Factor Ligand Superfamily Member 13 - antagonists & inhibitors</subject><subject>Tumor Necrosis Factor Ligand Superfamily Member 13 - immunology</subject><issn>0953-8178</issn><issn>1460-2377</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkDtPxDAQhC0EguNR0iKLgi5gx_GrPA4OEEg0ICGayE6Ww5A4IXaku4bfjhEHBdUW--3M7CB0SMkpJZqdOR9d257Vy4YosoEmtBAky5mUm2hCNGeZolLtoN0Q3gghLNdsG-1QoWnBiZqgzyk-n87n2PhoFp13IeIw9v0AIUDAsOxhcC2kZYPNGLtkNXrA4CvoX03TtStoXHQB2xWOZlhAdH6BK2iarIXamQh1kq7x69h2Q9JY3yf5vvPJYR9tvZgmwMF67qHH-eXD7Dq7u7-6mU3vMpczHrNKGqustlIrYYysGVda1mBBgCkKbpQQutIvNa1YTioqGMtBWi4ZK7iVxLI9dPKj2w_dxwghlq0L3zGNh24MJdUsFUfzBB7_A9-6cfApW2I4oVwJmaCjNTTa9GbZp47MsCp_a01A9gOkPmH5tzfDe5nOJS-vn55Lxgt-cStmJWVf9iCMTA</recordid><startdate>20061001</startdate><enddate>20061001</enddate><creator>Huntington, Nicholas D.</creator><creator>Tomioka, Ryo</creator><creator>Clavarino, Chelsea</creator><creator>Chow, Anne M.</creator><creator>Liñares, David</creator><creator>Maña, Paula</creator><creator>Rossjohn, Jamie</creator><creator>Cachero, Teresa G.</creator><creator>Qian, Fang</creator><creator>Kalled, Susan L.</creator><creator>Bernard, Claude C. A.</creator><creator>Reid, Hugh H.</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope></search><sort><creationdate>20061001</creationdate><title>A BAFF antagonist suppresses experimental autoimmune encephalomyelitis by targeting cell-mediated and humoral immune responses</title><author>Huntington, Nicholas D. ; Tomioka, Ryo ; Clavarino, Chelsea ; Chow, Anne M. ; Liñares, David ; Maña, Paula ; Rossjohn, Jamie ; Cachero, Teresa G. ; Qian, Fang ; Kalled, Susan L. ; Bernard, Claude C. 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A.</au><au>Reid, Hugh H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A BAFF antagonist suppresses experimental autoimmune encephalomyelitis by targeting cell-mediated and humoral immune responses</atitle><jtitle>International immunology</jtitle><addtitle>Int Immunol</addtitle><date>2006-10-01</date><risdate>2006</risdate><volume>18</volume><issue>10</issue><spage>1473</spage><epage>1485</epage><pages>1473-1485</pages><issn>0953-8178</issn><eissn>1460-2377</eissn><abstract>BAFF [B cell-activating factor of the tumour necrosis factor (TNF) family] and APRIL (a proliferation-inducing ligand) are two TNF family members with shared receptors. While, physiological roles for APRIL are not fully understood, BAFF is critical for B cell homeostasis and also acts as a co-stimulator of T cells. Using a B and T cell-mediated mouse model of multiple sclerosis (MS), myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), we observed that a BAFF/APRIL antagonist (soluble BCMA-Fc) inhibited central nervous system inflammation and demyelination such that it suppressed the onset and progression of clinical symptoms of EAE. In addition to dramatically reducing the titre of MOG-specific auto-antibodies, this treatment also induced a switch in the subtype of the Th cell population characterized by marked alterations in cytokine production following re-stimulation with MOG in vitro. Indeed, hBCMA-Fc therapy led to significant increases in the level of transforming growth factor β, while the levels of Th1 cytokines were markedly diminished. These results not only identify BAFF as a critical factor in maintaining humoral immunity in EAE but also support its role in T lymphocyte responses. Our findings demonstrate that hBCMA-Fc acts on both effector arms of the immune response in EAE, a characteristic that may be of significant therapeutic value in the treatment of MS.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>16914508</pmid><doi>10.1093/intimm/dxl080</doi><tpages>13</tpages></addata></record> |
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subjects | Animals Antibody Formation - drug effects Antibody Formation - immunology autoimmunity B-Cell Activating Factor - antagonists & inhibitors B-Cell Activating Factor - immunology B-Cell Maturation Antigen - administration & dosage B-Lymphocytes - immunology central nervous system diseases cytokine receptors cytokines Encephalomyelitis, Autoimmune, Experimental - chemically induced Encephalomyelitis, Autoimmune, Experimental - drug therapy Encephalomyelitis, Autoimmune, Experimental - immunology Female Immunity, Cellular - drug effects Immunity, Cellular - immunology Immunoglobulin Fc Fragments - administration & dosage Mice Mice, Inbred NOD multiple sclerosis Multiple Sclerosis - chemically induced Multiple Sclerosis - drug therapy Multiple Sclerosis - immunology Myelin Proteins Myelin-Associated Glycoprotein - administration & dosage Myelin-Associated Glycoprotein - toxicity Myelin-Oligodendrocyte Glycoprotein Recombinant Fusion Proteins - administration & dosage T-Lymphocytes - immunology therapeutics Tumor Necrosis Factor Ligand Superfamily Member 13 - antagonists & inhibitors Tumor Necrosis Factor Ligand Superfamily Member 13 - immunology |
title | A BAFF antagonist suppresses experimental autoimmune encephalomyelitis by targeting cell-mediated and humoral immune responses |
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