Infiltration of CD4+ lymphocytes into the brain contributes to neurodegeneration in a mouse model of Parkinson disease.
Identifieur interne : 000B94 ( PubMed/Curation ); précédent : 000B93; suivant : 000B95Infiltration of CD4+ lymphocytes into the brain contributes to neurodegeneration in a mouse model of Parkinson disease.
Auteurs : Vanessa Brochard [France] ; Béhazine Combadière ; Annick Prigent ; Yasmina Laouar ; Aline Perrin ; Virginie Beray-Berthat ; Olivia Bonduelle ; Daniel Alvarez-Fischer ; Jacques Callebert ; Jean-Marie Launay ; Charles Duyckaerts ; Richard A. Flavell ; Etienne C. Hirsch ; Stéphane HunotSource :
- The Journal of clinical investigation [ 0021-9738 ] ; 2009.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Animals, Brain (cytology), Brain (immunology), Brain (pathology), CD4-Positive T-Lymphocytes (cytology), CD4-Positive T-Lymphocytes (immunology), Cell Death (physiology), Disease Models, Animal, Dopamine (metabolism), Fas Ligand Protein (genetics), Fas Ligand Protein (metabolism), Homeodomain Proteins (genetics), Homeodomain Proteins (metabolism), Humans, Immune System (physiology), Interferon-gamma (metabolism), Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Nerve Degeneration (immunology), Nerve Degeneration (pathology), Neurons (cytology), Neurons (metabolism), Neurons (pathology), Parkinson Disease (immunology), Parkinson Disease (pathology), Parkinsonian Disorders (immunology), Parkinsonian Disorders (pathology).
- MESH :
- chemical , genetics : Fas Ligand Protein, Homeodomain Proteins.
- chemical , metabolism : Dopamine, Fas Ligand Protein, Homeodomain Proteins, Interferon-gamma.
- cytology : Brain, CD4-Positive T-Lymphocytes, Neurons.
- immunology : Brain, CD4-Positive T-Lymphocytes, Nerve Degeneration, Parkinson Disease, Parkinsonian Disorders.
- metabolism : Neurons.
- pathology : Brain, Nerve Degeneration, Neurons, Parkinson Disease, Parkinsonian Disorders.
- physiology : Cell Death, Immune System.
- Aged, Aged, 80 and over, Animals, Disease Models, Animal, Humans, Male, Mice, Mice, Inbred C57BL, Mice, Knockout.
Abstract
Parkinson disease (PD) is a neurodegenerative disorder characterized by a loss of dopamine-containing neurons. Mounting evidence suggests that dopaminergic cell death is influenced by the innate immune system. However, the pathogenic role of the adaptive immune system in PD remains enigmatic. Here we showed that CD8+ and CD4+ T cells but not B cells had invaded the brain in both postmortem human PD specimens and in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD during the course of neuronal degeneration. We further demonstrated that MPTP-induced dopaminergic cell death was markedly attenuated in the absence of mature T lymphocytes in 2 different immunodeficient mouse strains (Rag1-/- and Tcrb-/- mice). Importantly, similar attenuation of MPTP-induced dopaminergic cell death was seen in mice lacking CD4 as well as in Rag1-/- mice reconstituted with FasL-deficient splenocytes. However, mice lacking CD8 and Rag1-/- mice reconstituted with IFN-gamma-deficient splenocytes were not protected. These data indicate that T cell-mediated dopaminergic toxicity is almost exclusively arbitrated by CD4+ T cells and requires the expression of FasL but not IFNgamma. Further, our data may provide a rationale for targeting the adaptive arm of the immune system as a therapeutic strategy in PD.
DOI: 10.1172/JCI36470
PubMed: 19104149
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Flavell</name></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. Hirsch</name></author><author><name sortKey="Hunot, Stephane" sort="Hunot, Stephane" uniqKey="Hunot S" first="Stéphane" last="Hunot">Stéphane Hunot</name></author></analytic><series><title level="j">The Journal of clinical investigation</title><idno type="ISSN">0021-9738</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Animals</term><term>Brain (cytology)</term><term>Brain (immunology)</term><term>Brain (pathology)</term><term>CD4-Positive T-Lymphocytes (cytology)</term><term>CD4-Positive T-Lymphocytes (immunology)</term><term>Cell Death (physiology)</term><term>Disease Models, Animal</term><term>Dopamine (metabolism)</term><term>Fas Ligand Protein (genetics)</term><term>Fas Ligand Protein (metabolism)</term><term>Homeodomain Proteins (genetics)</term><term>Homeodomain Proteins (metabolism)</term><term>Humans</term><term>Immune System (physiology)</term><term>Interferon-gamma (metabolism)</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Nerve Degeneration (immunology)</term><term>Nerve Degeneration (pathology)</term><term>Neurons (cytology)</term><term>Neurons (metabolism)</term><term>Neurons (pathology)</term><term>Parkinson Disease (immunology)</term><term>Parkinson Disease (pathology)</term><term>Parkinsonian Disorders (immunology)</term><term>Parkinsonian Disorders (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Fas Ligand Protein</term><term>Homeodomain Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Fas Ligand Protein</term><term>Homeodomain Proteins</term><term>Interferon-gamma</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Brain</term><term>CD4-Positive T-Lymphocytes</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Brain</term><term>CD4-Positive T-Lymphocytes</term><term>Nerve Degeneration</term><term>Parkinson Disease</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Nerve Degeneration</term><term>Neurons</term><term>Parkinson Disease</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Death</term><term>Immune System</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson disease (PD) is a neurodegenerative disorder characterized by a loss of dopamine-containing neurons. Mounting evidence suggests that dopaminergic cell death is influenced by the innate immune system. However, the pathogenic role of the adaptive immune system in PD remains enigmatic. Here we showed that CD8+ and CD4+ T cells but not B cells had invaded the brain in both postmortem human PD specimens and in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD during the course of neuronal degeneration. We further demonstrated that MPTP-induced dopaminergic cell death was markedly attenuated in the absence of mature T lymphocytes in 2 different immunodeficient mouse strains (Rag1-/- and Tcrb-/- mice). Importantly, similar attenuation of MPTP-induced dopaminergic cell death was seen in mice lacking CD4 as well as in Rag1-/- mice reconstituted with FasL-deficient splenocytes. However, mice lacking CD8 and Rag1-/- mice reconstituted with IFN-gamma-deficient splenocytes were not protected. These data indicate that T cell-mediated dopaminergic toxicity is almost exclusively arbitrated by CD4+ T cells and requires the expression of FasL but not IFNgamma. Further, our data may provide a rationale for targeting the adaptive arm of the immune system as a therapeutic strategy in PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19104149</PMID><DateCreated><Year>2009</Year><Month>01</Month><Day>07</Day></DateCreated><DateCompleted><Year>2009</Year><Month>03</Month><Day>10</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0021-9738</ISSN><JournalIssue CitedMedium="Print"><Volume>119</Volume><Issue>1</Issue><PubDate><Year>2009</Year><Month>Jan</Month></PubDate></JournalIssue><Title>The Journal of clinical investigation</Title><ISOAbbreviation>J. Clin. Invest.</ISOAbbreviation></Journal><ArticleTitle>Infiltration of CD4+ lymphocytes into the brain contributes to neurodegeneration in a mouse model of Parkinson disease.</ArticleTitle><Pagination><MedlinePgn>182-92</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1172/JCI36470</ELocationID><ELocationID EIdType="pii" ValidYN="Y">36470</ELocationID><Abstract><AbstractText>Parkinson disease (PD) is a neurodegenerative disorder characterized by a loss of dopamine-containing neurons. Mounting evidence suggests that dopaminergic cell death is influenced by the innate immune system. However, the pathogenic role of the adaptive immune system in PD remains enigmatic. Here we showed that CD8+ and CD4+ T cells but not B cells had invaded the brain in both postmortem human PD specimens and in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD during the course of neuronal degeneration. We further demonstrated that MPTP-induced dopaminergic cell death was markedly attenuated in the absence of mature T lymphocytes in 2 different immunodeficient mouse strains (Rag1-/- and Tcrb-/- mice). Importantly, similar attenuation of MPTP-induced dopaminergic cell death was seen in mice lacking CD4 as well as in Rag1-/- mice reconstituted with FasL-deficient splenocytes. However, mice lacking CD8 and Rag1-/- mice reconstituted with IFN-gamma-deficient splenocytes were not protected. These data indicate that T cell-mediated dopaminergic toxicity is almost exclusively arbitrated by CD4+ T cells and requires the expression of FasL but not IFNgamma. Further, our data may provide a rationale for targeting the adaptive arm of the immune system as a therapeutic strategy in PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Brochard</LastName><ForeName>Vanessa</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>INSERM, UMR S679, Experimental Neurology and Therapeutics, Hopital de la Salpetriere, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Combadière</LastName><ForeName>Béhazine</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Prigent</LastName><ForeName>Annick</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Laouar</LastName><ForeName>Yasmina</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Perrin</LastName><ForeName>Aline</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Beray-Berthat</LastName><ForeName>Virginie</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Bonduelle</LastName><ForeName>Olivia</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Alvarez-Fischer</LastName><ForeName>Daniel</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Callebert</LastName><ForeName>Jacques</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Launay</LastName><ForeName>Jean-Marie</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Duyckaerts</LastName><ForeName>Charles</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Flavell</LastName><ForeName>Richard A</ForeName><Initials>RA</Initials></Author><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>Etienne C</ForeName><Initials>EC</Initials></Author><Author ValidYN="Y"><LastName>Hunot</LastName><ForeName>Stéphane</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Howard Hughes Medical Institute</Agency><Country>United States</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>2008</Year><Month>12</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Clin Invest</MedlineTA><NlmUniqueID>7802877</NlmUniqueID><ISSNLinking>0021-9738</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053222">Fas Ligand Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C505658">Fasl protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018398">Homeodomain Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>128559-51-3</RegistryNumber><NameOfSubstance UI="C064658">RAG-1 protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>82115-62-6</RegistryNumber><NameOfSubstance UI="D007371">Interferon-gamma</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 1994 May 10;91(10):4185-9</RefSource><PMID Version="1">7514297</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell. 1994 Mar 25;76(6):969-76</RefSource><PMID Version="1">7511063</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurodegeneration. 1996 Dec;5(4):299-312</RefSource><PMID Version="1">9117541</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7531-6</RefSource><PMID 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