Involvement of the Fc gamma receptor in a chronic N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of dopaminergic loss.
Identifieur interne : 000B86 ( PubMed/Corpus ); précédent : 000B85; suivant : 000B87Involvement of the Fc gamma receptor in a chronic N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of dopaminergic loss.
Auteurs : Arman Lira ; Jerzy Kulczycki ; Ruth Slack ; Hymie Anisman ; David S. ParkSource :
- The Journal of biological chemistry [ 1083-351X ] ; 2011.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (adverse effects), 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pharmacology), Animals, Cell Death (drug effects), Cell Death (genetics), Cell Death (immunology), DNA-Binding Proteins (genetics), DNA-Binding Proteins (immunology), DNA-Binding Proteins (metabolism), Disease Models, Animal, Immunoglobulin G (genetics), Immunoglobulin G (immunology), Immunoglobulin G (metabolism), MPTP Poisoning (genetics), MPTP Poisoning (immunology), MPTP Poisoning (metabolism), Mice, Mice, Knockout, Neurotoxins (adverse effects), Neurotoxins (pharmacology), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (genetics), Parkinson Disease, Secondary (immunology), Receptors, IgG (genetics), Receptors, IgG (immunology), Receptors, IgG (metabolism).
- MESH :
- chemical , adverse effects : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Neurotoxins.
- chemical , genetics : DNA-Binding Proteins, Immunoglobulin G, Receptors, IgG.
- chemical , immunology : DNA-Binding Proteins, Immunoglobulin G, Receptors, IgG.
- chemical , metabolism : DNA-Binding Proteins, Immunoglobulin G, Receptors, IgG.
- chemical , pharmacology : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Neurotoxins.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Cell Death.
- genetics : Cell Death, MPTP Poisoning, Parkinson Disease, Secondary.
- immunology : Cell Death, MPTP Poisoning, Parkinson Disease, Secondary.
- metabolism : MPTP Poisoning.
- Animals, Disease Models, Animal, Mice, Mice, Knockout.
Abstract
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.
DOI: 10.1074/jbc.M111.244830
PubMed: 21693708
Links to Exploration step
pubmed:21693708Le document en format XML
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Park</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2011">2011</date><idno type="RBID">pubmed:21693708</idno><idno type="pmid">21693708</idno><idno type="doi">10.1074/jbc.M111.244830</idno><idno type="wicri:Area/PubMed/Corpus">000B86</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000B86</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Involvement of the Fc gamma receptor in a chronic N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of dopaminergic loss.</title><author><name sortKey="Lira, Arman" sort="Lira, Arman" uniqKey="Lira A" first="Arman" last="Lira">Arman Lira</name><affiliation><nlm:affiliation>Department of Cellular Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Kulczycki, Jerzy" sort="Kulczycki, Jerzy" uniqKey="Kulczycki J" first="Jerzy" last="Kulczycki">Jerzy Kulczycki</name></author><author><name sortKey="Slack, Ruth" sort="Slack, Ruth" uniqKey="Slack R" first="Ruth" last="Slack">Ruth Slack</name></author><author><name sortKey="Anisman, Hymie" sort="Anisman, Hymie" uniqKey="Anisman H" first="Hymie" last="Anisman">Hymie Anisman</name></author><author><name sortKey="Park, David S" sort="Park, David S" uniqKey="Park D" first="David S" last="Park">David S. Park</name></author></analytic><series><title level="j">The Journal of biological chemistry</title><idno type="eISSN">1083-351X</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (adverse effects)</term><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pharmacology)</term><term>Animals</term><term>Cell Death (drug effects)</term><term>Cell Death (genetics)</term><term>Cell Death (immunology)</term><term>DNA-Binding Proteins (genetics)</term><term>DNA-Binding Proteins (immunology)</term><term>DNA-Binding Proteins (metabolism)</term><term>Disease Models, Animal</term><term>Immunoglobulin G (genetics)</term><term>Immunoglobulin G (immunology)</term><term>Immunoglobulin G (metabolism)</term><term>MPTP Poisoning (genetics)</term><term>MPTP Poisoning (immunology)</term><term>MPTP Poisoning (metabolism)</term><term>Mice</term><term>Mice, Knockout</term><term>Neurotoxins (adverse effects)</term><term>Neurotoxins (pharmacology)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (genetics)</term><term>Parkinson Disease, Secondary (immunology)</term><term>Receptors, IgG (genetics)</term><term>Receptors, IgG (immunology)</term><term>Receptors, IgG (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Neurotoxins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA-Binding Proteins</term><term>Immunoglobulin G</term><term>Receptors, IgG</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>DNA-Binding Proteins</term><term>Immunoglobulin G</term><term>Receptors, IgG</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>DNA-Binding Proteins</term><term>Immunoglobulin G</term><term>Receptors, IgG</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Neurotoxins</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Death</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Death</term><term>MPTP Poisoning</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Cell Death</term><term>MPTP Poisoning</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>MPTP Poisoning</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Mice</term><term>Mice, Knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21693708</PMID><DateCreated><Year>2011</Year><Month>08</Month><Day>15</Day></DateCreated><DateCompleted><Year>2011</Year><Month>10</Month><Day>19</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1083-351X</ISSN><JournalIssue CitedMedium="Internet"><Volume>286</Volume><Issue>33</Issue><PubDate><Year>2011</Year><Month>Aug</Month><Day>19</Day></PubDate></JournalIssue><Title>The Journal of biological chemistry</Title><ISOAbbreviation>J. Biol. Chem.</ISOAbbreviation></Journal><ArticleTitle>Involvement of the Fc gamma receptor in a chronic N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of dopaminergic loss.</ArticleTitle><Pagination><MedlinePgn>28783-93</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1074/jbc.M111.244830</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lira</LastName><ForeName>Arman</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cellular Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kulczycki</LastName><ForeName>Jerzy</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Slack</LastName><ForeName>Ruth</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Anisman</LastName><ForeName>Hymie</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>David S</ForeName><Initials>DS</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>06</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Biol Chem</MedlineTA><NlmUniqueID>2985121R</NlmUniqueID><ISSNLinking>0021-9258</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004268">DNA-Binding Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007074">Immunoglobulin G</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009498">Neurotoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C499308">Rag2 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017452">Receptors, IgG</NameOfSubstance></Chemical><Chemical><RegistryNumber>9P21XSP91P</RegistryNumber><NameOfSubstance UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>FASEB J. 2005 Mar;19(3):407-9</RefSource><PMID Version="1">15625078</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Acta Neurobiol Exp (Wars). 1999;59(1):1-8</RefSource><PMID Version="1">10230070</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur J Neurosci. 1996 Feb;8(2):365-81</RefSource><PMID Version="1">8714707</PMID></CommentsCorrections><CommentsCorrections 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