B cells limit epitope spreading and reduce severity of EAE induced with PLP peptide in BALB/c mice
Abstract The role of B cells and antibody in experimental autoimmune encephalomyelitis (EAE) appears to differ based on the identity and state (protein vs. encephalitogenic peptide) of the inducing antigen and the strain of mouse utilized. The involvement of B cells in the induction of EAE by peptid...
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| Veröffentlicht in: | Journal of autoimmunity 2008-09, Vol.31 (2), p.149-155 |
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| description | Abstract The role of B cells and antibody in experimental autoimmune encephalomyelitis (EAE) appears to differ based on the identity and state (protein vs. encephalitogenic peptide) of the inducing antigen and the strain of mouse utilized. The involvement of B cells in the induction of EAE by peptides of proteolipid protein (PLP) in BALB/c mice was investigated. Wild-type and B cell-deficient (B cell−/− ) mice on the BALB/c background were immunized with overlapping PLP peptides, and the disease course was followed. Although incidence and onset of PLP180–199 -induced EAE was similar in WT and B cell−/− mice, the clinical course was more severe in B cell−/− mice. During acute disease, proliferation and interferon-γ production by lymphoid cells from both strains were similar and were elicited predominantly in response to the immunizing antigen. However, during chronic disease lymphoid cells isolated from B cell−/− mice proliferated to a greater extent and produced more interferon-γ in response to the overlapping peptide PLP185–206 and to the smaller internal peptide PLP185–199 than did WT mice. These data suggest that B cells regulate PLP-induced EAE in BALB/c mice through control of epitope spreading. |
| doi_str_mv | 10.1016/j.jaut.2008.04.025 |
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The involvement of B cells in the induction of EAE by peptides of proteolipid protein (PLP) in BALB/c mice was investigated. Wild-type and B cell-deficient (B cell−/− ) mice on the BALB/c background were immunized with overlapping PLP peptides, and the disease course was followed. Although incidence and onset of PLP180–199 -induced EAE was similar in WT and B cell−/− mice, the clinical course was more severe in B cell−/− mice. During acute disease, proliferation and interferon-γ production by lymphoid cells from both strains were similar and were elicited predominantly in response to the immunizing antigen. However, during chronic disease lymphoid cells isolated from B cell−/− mice proliferated to a greater extent and produced more interferon-γ in response to the overlapping peptide PLP185–206 and to the smaller internal peptide PLP185–199 than did WT mice. These data suggest that B cells regulate PLP-induced EAE in BALB/c mice through control of epitope spreading.</description><identifier>ISSN: 0896-8411</identifier><identifier>EISSN: 1095-9157</identifier><identifier>DOI: 10.1016/j.jaut.2008.04.025</identifier><identifier>PMID: 18539432</identifier><language>eng</language><publisher>London: Elsevier Ltd</publisher><subject>Allergy and Immunology ; Amino Acid Sequence ; Animals ; Antibody ; B cells ; B-Lymphocytes - immunology ; Biological and medical sciences ; Encephalomyelitis, Autoimmune, Experimental - chemically induced ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Encephalomyelitis, Autoimmune, Experimental - physiopathology ; Enzyme-Linked Immunosorbent Assay ; Epitope spreading ; Epitopes - immunology ; Experimental autoimmune encephalomyelitis ; Female ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Molecular Sequence Data ; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis ; Myelin Proteolipid Protein - genetics ; Myelin Proteolipid Protein - immunology ; Neurology ; Peptides - genetics ; Peptides - immunology ; Peptides - pharmacology ; Proteolipid protein ; Severity of Illness Index</subject><ispartof>Journal of autoimmunity, 2008-09, Vol.31 (2), p.149-155</ispartof><rights>Elsevier Ltd</rights><rights>2008 Elsevier Ltd</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c569t-7de0e6a0e8baa39e706f6bcb076e312f975b9145c5a0d3910472dd781ec695363</citedby><cites>FETCH-LOGICAL-c569t-7de0e6a0e8baa39e706f6bcb076e312f975b9145c5a0d3910472dd781ec695363</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jaut.2008.04.025$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20706925$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18539432$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lyons, Jeri-Anne</creatorcontrib><creatorcontrib>Ramsbottom, Michael J</creatorcontrib><creatorcontrib>Mikesell, Robert J</creatorcontrib><creatorcontrib>Cross, Anne H</creatorcontrib><title>B cells limit epitope spreading and reduce severity of EAE induced with PLP peptide in BALB/c mice</title><title>Journal of autoimmunity</title><addtitle>J Autoimmun</addtitle><description>Abstract The role of B cells and antibody in experimental autoimmune encephalomyelitis (EAE) appears to differ based on the identity and state (protein vs. encephalitogenic peptide) of the inducing antigen and the strain of mouse utilized. The involvement of B cells in the induction of EAE by peptides of proteolipid protein (PLP) in BALB/c mice was investigated. Wild-type and B cell-deficient (B cell−/− ) mice on the BALB/c background were immunized with overlapping PLP peptides, and the disease course was followed. Although incidence and onset of PLP180–199 -induced EAE was similar in WT and B cell−/− mice, the clinical course was more severe in B cell−/− mice. During acute disease, proliferation and interferon-γ production by lymphoid cells from both strains were similar and were elicited predominantly in response to the immunizing antigen. However, during chronic disease lymphoid cells isolated from B cell−/− mice proliferated to a greater extent and produced more interferon-γ in response to the overlapping peptide PLP185–206 and to the smaller internal peptide PLP185–199 than did WT mice. These data suggest that B cells regulate PLP-induced EAE in BALB/c mice through control of epitope spreading.</description><subject>Allergy and Immunology</subject><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Antibody</subject><subject>B cells</subject><subject>B-Lymphocytes - immunology</subject><subject>Biological and medical sciences</subject><subject>Encephalomyelitis, Autoimmune, Experimental - chemically induced</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Encephalomyelitis, Autoimmune, Experimental - physiopathology</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Epitope spreading</subject><subject>Epitopes - immunology</subject><subject>Experimental autoimmune encephalomyelitis</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Knockout</subject><subject>Molecular Sequence Data</subject><subject>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</subject><subject>Myelin Proteolipid Protein - genetics</subject><subject>Myelin Proteolipid Protein - immunology</subject><subject>Neurology</subject><subject>Peptides - genetics</subject><subject>Peptides - immunology</subject><subject>Peptides - pharmacology</subject><subject>Proteolipid protein</subject><subject>Severity of Illness Index</subject><issn>0896-8411</issn><issn>1095-9157</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kk1v1DAQhiMEokvhD3BAvsAt6diJk1hClXarLSCtRCVA4mY59qR1yFftZNH-e5zuqnwcOI008847o3kmil5TSCjQ_KJJGjVPCQMoE8gSYPxJtKIgeCwoL55GKyhFHpcZpWfRC-8bAEo558-jM1ryVGQpW0XVhmhsW09a29mJ4GinYUTiR4fK2P6WqN4Qh2bWIYl7dHY6kKEm2_WW2H5JG_LTTnfkZndDRhwnazAUyGa921xo0lmNL6NntWo9vjrF8-jb9fbr1cd49_nDp6v1LtY8F1NcGATMFWBZKZUKLCCv80pXUOSYUlaLgleCZlxzBSYVFLKCGVOUFHUueJqn59Hl0Xecqw6Nxn5yqpWjs51yBzkoK_-u9PZO3g57yXgJRSGCwbuTgRvuZ_ST7KxfrqN6HGYvGQgqeMaCkB2F2g3eO6wfh1CQCxrZyAWNXNBIyGRAE5re_Lne75YTiyB4exIor1VbO9Vr6x91DMJFxIPR-6MOwzH3Fp302mIfSFiHepJmsP_f4_Kfdt3a3oaJP_CAvhlm1wdMkkrPJMgvyxMtPwQlQFjhe_oLs1nBtA</recordid><startdate>20080901</startdate><enddate>20080901</enddate><creator>Lyons, Jeri-Anne</creator><creator>Ramsbottom, Michael J</creator><creator>Mikesell, Robert J</creator><creator>Cross, Anne H</creator><general>Elsevier Ltd</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>5PM</scope></search><sort><creationdate>20080901</creationdate><title>B cells limit epitope spreading and reduce severity of EAE induced with PLP peptide in BALB/c mice</title><author>Lyons, Jeri-Anne ; Ramsbottom, Michael J ; Mikesell, Robert J ; Cross, Anne H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c569t-7de0e6a0e8baa39e706f6bcb076e312f975b9145c5a0d3910472dd781ec695363</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Allergy and Immunology</topic><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>Antibody</topic><topic>B cells</topic><topic>B-Lymphocytes - immunology</topic><topic>Biological and medical sciences</topic><topic>Encephalomyelitis, Autoimmune, Experimental - chemically induced</topic><topic>Encephalomyelitis, Autoimmune, Experimental - immunology</topic><topic>Encephalomyelitis, Autoimmune, Experimental - physiopathology</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Epitope spreading</topic><topic>Epitopes - immunology</topic><topic>Experimental autoimmune encephalomyelitis</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Knockout</topic><topic>Molecular Sequence Data</topic><topic>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</topic><topic>Myelin Proteolipid Protein - genetics</topic><topic>Myelin Proteolipid Protein - immunology</topic><topic>Neurology</topic><topic>Peptides - genetics</topic><topic>Peptides - immunology</topic><topic>Peptides - pharmacology</topic><topic>Proteolipid protein</topic><topic>Severity of Illness Index</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lyons, Jeri-Anne</creatorcontrib><creatorcontrib>Ramsbottom, Michael J</creatorcontrib><creatorcontrib>Mikesell, Robert J</creatorcontrib><creatorcontrib>Cross, Anne H</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>PubMed Central (Full Participant titles)</collection><jtitle>Journal of autoimmunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lyons, Jeri-Anne</au><au>Ramsbottom, Michael J</au><au>Mikesell, Robert J</au><au>Cross, Anne H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>B cells limit epitope spreading and reduce severity of EAE induced with PLP peptide in BALB/c mice</atitle><jtitle>Journal of autoimmunity</jtitle><addtitle>J Autoimmun</addtitle><date>2008-09-01</date><risdate>2008</risdate><volume>31</volume><issue>2</issue><spage>149</spage><epage>155</epage><pages>149-155</pages><issn>0896-8411</issn><eissn>1095-9157</eissn><abstract>Abstract The role of B cells and antibody in experimental autoimmune encephalomyelitis (EAE) appears to differ based on the identity and state (protein vs. encephalitogenic peptide) of the inducing antigen and the strain of mouse utilized. The involvement of B cells in the induction of EAE by peptides of proteolipid protein (PLP) in BALB/c mice was investigated. Wild-type and B cell-deficient (B cell−/− ) mice on the BALB/c background were immunized with overlapping PLP peptides, and the disease course was followed. Although incidence and onset of PLP180–199 -induced EAE was similar in WT and B cell−/− mice, the clinical course was more severe in B cell−/− mice. During acute disease, proliferation and interferon-γ production by lymphoid cells from both strains were similar and were elicited predominantly in response to the immunizing antigen. However, during chronic disease lymphoid cells isolated from B cell−/− mice proliferated to a greater extent and produced more interferon-γ in response to the overlapping peptide PLP185–206 and to the smaller internal peptide PLP185–199 than did WT mice. These data suggest that B cells regulate PLP-induced EAE in BALB/c mice through control of epitope spreading.</abstract><cop>London</cop><pub>Elsevier Ltd</pub><pmid>18539432</pmid><doi>10.1016/j.jaut.2008.04.025</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of autoimmunity, 2008-09, Vol.31 (2), p.149-155 |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Allergy and Immunology Amino Acid Sequence Animals Antibody B cells B-Lymphocytes - immunology Biological and medical sciences Encephalomyelitis, Autoimmune, Experimental - chemically induced Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - physiopathology Enzyme-Linked Immunosorbent Assay Epitope spreading Epitopes - immunology Experimental autoimmune encephalomyelitis Female Fundamental and applied biological sciences. Psychology Fundamental immunology Medical sciences Mice Mice, Inbred BALB C Mice, Knockout Molecular Sequence Data Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis Myelin Proteolipid Protein - genetics Myelin Proteolipid Protein - immunology Neurology Peptides - genetics Peptides - immunology Peptides - pharmacology Proteolipid protein Severity of Illness Index |
| title | B cells limit epitope spreading and reduce severity of EAE induced with PLP peptide in BALB/c mice |
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