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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Involvement of the Fcγ Receptor in a Chronic <italic>N</italic>-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Mouse Model of Dopaminergic Loss<xref ref-type="fn" rid="FN1">*</xref></title><author><name sortKey="Lira, Arman" sort="Lira, Arman" uniqKey="Lira A" first="Arman" last="Lira">Arman Lira</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Kulczycki, Jerzy" sort="Kulczycki, Jerzy" uniqKey="Kulczycki J" first="Jerzy" last="Kulczycki">Jerzy Kulczycki</name><affiliation><nlm:aff id="aff2"></nlm:aff></affiliation></author><author><name sortKey="Slack, Ruth" sort="Slack, Ruth" uniqKey="Slack R" first="Ruth" last="Slack">Ruth Slack</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Anisman, Hymie" sort="Anisman, Hymie" uniqKey="Anisman H" first="Hymie" last="Anisman">Hymie Anisman</name><affiliation><nlm:aff id="aff2"></nlm:aff></affiliation></author><author><name sortKey="Park, David S" sort="Park, David S" uniqKey="Park D" first="David S." last="Park">David S. Park</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff3"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">21693708</idno><idno type="pmc">3190686</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3190686</idno><idno type="RBID">PMC:3190686</idno><idno type="doi">10.1074/jbc.M111.244830</idno><date when="2011">2011</date><idno type="wicri:Area/Pmc/Corpus">000559</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000559</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Involvement of the Fcγ Receptor in a Chronic <italic>N</italic>-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Mouse Model of Dopaminergic Loss<xref ref-type="fn" rid="FN1">*</xref></title><author><name sortKey="Lira, Arman" sort="Lira, Arman" uniqKey="Lira A" first="Arman" last="Lira">Arman Lira</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Kulczycki, Jerzy" sort="Kulczycki, Jerzy" uniqKey="Kulczycki J" first="Jerzy" last="Kulczycki">Jerzy Kulczycki</name><affiliation><nlm:aff id="aff2"></nlm:aff></affiliation></author><author><name sortKey="Slack, Ruth" sort="Slack, Ruth" uniqKey="Slack R" first="Ruth" last="Slack">Ruth Slack</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Anisman, Hymie" sort="Anisman, Hymie" uniqKey="Anisman H" first="Hymie" last="Anisman">Hymie Anisman</name><affiliation><nlm:aff id="aff2"></nlm:aff></affiliation></author><author><name sortKey="Park, David S" sort="Park, David S" uniqKey="Park D" first="David S." last="Park">David S. Park</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff3"></nlm:aff></affiliation></author></analytic><series><title level="j">The Journal of Biological Chemistry</title><idno type="ISSN">0021-9258</idno><idno type="eISSN">1083-351X</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Although there is growing evidence for a role of the innate immune response in Parkinson's disease, the nature of any humoral response in dopaminergic degeneration is uncertain. Here we report on a protracted N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of dopaminergic death that potentially allows a more full adaptive humoral response to develop. Rag2 mutant mice that lack the full adaptive response (deficient in both T and B cells) are resistant to dopaminergic death and behavioral deficiencies in this model. These mice are resensitized after reconstitution with WT splenocytes. To more directly provide evidence for humoral/IgG involvement, we show that deficiency of Fcγ receptors, which are critical for activation of macrophages/microglia by binding to IgGs, is also protective in this protracted model. FcγR-deficient mice display improved behavior and impaired microglial activation. Interestingly, however, Rag2 mutant but not FcγR-deficient mice are resistant to a more standard N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine paradigm where death is more rapid. Taken together, these data indicate that, provided sufficient time, the humoral arm of the adaptive immune system can play a critical functional role in modulating the microglial response to dopaminergic degeneration and suggest that this humoral component may participate in degeneration in Parkinson's disease.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Biol Chem</journal-id><journal-id journal-id-type="hwp">jbc</journal-id><journal-id journal-id-type="pmc">jbc</journal-id><journal-id journal-id-type="publisher-id">JBC</journal-id><journal-title-group><journal-title>The Journal of Biological Chemistry</journal-title></journal-title-group><issn pub-type="ppub">0021-9258</issn><issn pub-type="epub">1083-351X</issn><publisher><publisher-name>American Society for Biochemistry and Molecular Biology</publisher-name><publisher-loc>9650 Rockville Pike, Bethesda, MD 20814, U.S.A.</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">21693708</article-id><article-id pub-id-type="pmc">3190686</article-id><article-id pub-id-type="publisher-id">M111.244830</article-id><article-id pub-id-type="doi">10.1074/jbc.M111.244830</article-id><article-categories><subj-group subj-group-type="heading"><subject>Molecular Bases of Disease</subject></subj-group></article-categories><title-group><article-title>Involvement of the Fcγ Receptor in a Chronic <italic>N</italic>-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Mouse Model of Dopaminergic Loss<xref ref-type="fn" rid="FN1">*</xref></article-title><alt-title alt-title-type="short">Fcγ Receptor in Dopaminergic Loss</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Lira</surname><given-names>Arman</given-names></name><xref ref-type="aff" rid="aff1"><sup>‡</sup></xref></contrib><contrib contrib-type="author"><name><surname>Kulczycki</surname><given-names>Jerzy</given-names></name><xref ref-type="aff" rid="aff2"><sup>§</sup></xref></contrib><contrib contrib-type="author"><name><surname>Slack</surname><given-names>Ruth</given-names></name><xref ref-type="aff" rid="aff1"><sup>‡</sup></xref></contrib><contrib contrib-type="author"><name><surname>Anisman</surname><given-names>Hymie</given-names></name><xref ref-type="aff" rid="aff2"><sup>§</sup></xref></contrib><contrib contrib-type="author"><name><surname>Park</surname><given-names>David S.</given-names></name><xref ref-type="aff" rid="aff1"><sup>‡</sup></xref><xref ref-type="aff" rid="aff3"><sup>¶</sup></xref><xref ref-type="corresp" rid="cor1"><sup>1</sup></xref></contrib><aff id="aff1">From the<label>‡</label>Department of Cellular Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada,</aff><aff id="aff2">the<label>§</label>Institute of Neuroscience, Carleton University, Ottawa, Ontario K1S 5B6, Canada, and</aff><aff id="aff3">the<label>¶</label>Department of Cogno-Mechatronics Engineering, Pusan National University, Korea</aff></contrib-group><author-notes><corresp id="cor1"><label>1</label> To whom correspondence should be addressed: <addr-line>Department of Cellular and Molecular Medicine, University of Ottawa, 451 Smyth Rd., Ottawa, Ontario K1H 8M5, Canada.</addr-line> Fax: <fax>1-613-562-5403</fax>; E-mail: <email>dpark@uottawa.ca</email>.</corresp></author-notes><pub-date pub-type="ppub"><day>19</day><month>8</month><year>2011</year></pub-date><pub-date pub-type="epub"><day>21</day><month>6</month><year>2011</year></pub-date><volume>286</volume><issue>33</issue><fpage>28783</fpage><lpage>28793</lpage><history><date date-type="received"><day>30</day><month>3</month><year>2011</year></date><date date-type="rev-recd"><day>6</day><month>6</month><year>2011</year></date></history><permissions><copyright-statement>© 2011 by The American Society for Biochemistry and Molecular Biology, Inc.</copyright-statement><copyright-year>2011</copyright-year></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zbc03311028783.pdf"></self-uri><abstract><p>Although there is growing evidence for a role of the innate immune response in Parkinson's disease, the nature of any humoral response in dopaminergic degeneration is uncertain. Here we report on a protracted N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of dopaminergic death that potentially allows a more full adaptive humoral response to develop. Rag2 mutant mice that lack the full adaptive response (deficient in both T and B cells) are resistant to dopaminergic death and behavioral deficiencies in this model. These mice are resensitized after reconstitution with WT splenocytes. To more directly provide evidence for humoral/IgG involvement, we show that deficiency of Fcγ receptors, which are critical for activation of macrophages/microglia by binding to IgGs, is also protective in this protracted model. FcγR-deficient mice display improved behavior and impaired microglial activation. Interestingly, however, Rag2 mutant but not FcγR-deficient mice are resistant to a more standard N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine paradigm where death is more rapid. Taken together, these data indicate that, provided sufficient time, the humoral arm of the adaptive immune system can play a critical functional role in modulating the microglial response to dopaminergic degeneration and suggest that this humoral component may participate in degeneration in Parkinson's disease.</p></abstract><kwd-group><kwd>Humoral Response</kwd><kwd>Immunodeficiency</kwd><kwd>Lymphocyte</kwd><kwd>Neurodegeneration</kwd><kwd>Parkinson's Disease</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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