Autoimmunity to hypocretin and molecular mimicry to flu in type 1 narcolepsy.
Identifieur interne : 000012 ( PubMed/Corpus ); précédent : 000011; suivant : 000013Autoimmunity to hypocretin and molecular mimicry to flu in type 1 narcolepsy.
Auteurs : Guo Luo ; Aditya Ambati ; Ling Lin ; Mélodie Bonvalet ; Markku Partinen ; Xuhuai Ji ; Holden Terry Maecker ; Emmanuel Jean-Marie MignotSource :
- Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2018.
English descriptors
- KwdEn :
- Adolescent, Adult, Autoantigens (metabolism), Autoimmunity (immunology), CD4-Positive T-Lymphocytes (immunology), Child, Epitopes (immunology), Female, HLA-DQ beta-Chains, Hemagglutinins, Humans, Influenza A Virus, H1N1 Subtype (immunology), Influenza A virus (immunology), Influenza A virus (pathogenicity), Influenza, Human (immunology), Intracellular Signaling Peptides and Proteins (genetics), Male, Middle Aged, Molecular Mimicry (immunology), Narcolepsy (immunology), Orexins (genetics), Orexins (immunology), Orexins (metabolism), Peptides (genetics), Receptors, Antigen, T-Cell (genetics), Vaccination.
- MESH :
- chemical , genetics : Intracellular Signaling Peptides and Proteins, Orexins, Peptides, Receptors, Antigen, T-Cell.
- chemical , immunology : Epitopes, Orexins.
- chemical , metabolism : Autoantigens, Orexins.
- immunology : Autoimmunity, CD4-Positive T-Lymphocytes, Influenza A Virus, H1N1 Subtype, Influenza A virus, Influenza, Human, Molecular Mimicry, Narcolepsy.
- pathogenicity : Influenza A virus.
- Adolescent, Adult, Child, Female, HLA-DQ beta-Chains, Hemagglutinins, Humans, Male, Middle Aged, Vaccination.
Abstract
Type 1 narcolepsy (T1N) is caused by hypocretin/orexin (HCRT) neuronal loss. Association with the HLA DQB1*06:02/DQA1*01:02 (98% vs. 25%) heterodimer (DQ0602), T cell receptors (TCR) and other immune loci suggest autoimmunity but autoantigens are unknown. Onset is seasonal and associated with influenza A, notably pandemic 2009 H1N1 (pH1N1) infection and vaccination (Pandemrix). Peptides derived from HCRT and influenza A, including pH1N1, were screened for DQ0602 binding and presence of cognate DQ0602 tetramer-peptide-specific CD4+ T cells tested in 35 T1N cases and 22 DQ0602 controls. Higher reactivity to influenza pHA273-287 (pH1N1 specific), PR8 (H1N1 pre-2009 and H2N2)-specific NP17-31 and C-amidated but not native version of HCRT54-66 and HCRT86-97 (HCRTNH2) were observed in T1N. Single-cell TCR sequencing revealed sharing of CDR3β TRBV4-2-CASSQETQGRNYGYTF in HCRTNH2 and pHA273-287-tetramers, suggesting molecular mimicry. This public CDR3β uses TRBV4-2, a segment modulated by T1N-associated SNP rs1008599, suggesting causality. TCR-α/β CDR3 motifs of HCRT54-66-NH2 and HCRT86-97-NH2 tetramers were extensively shared: notably public CDR3α, TRAV2-CAVETDSWGKLQF-TRAJ24, that uses TRAJ24, a chain modulated by T1N-associated SNPs rs1154155 and rs1483979. TCR-α/β CDR3 sequences found in pHA273-287, NP17-31, and HCRTNH2 tetramer-positive CD4+ cells were also retrieved in single INF-γ-secreting CD4+ sorted cells stimulated with Pandemrix, independently confirming these results. Our results provide evidence for autoimmunity and molecular mimicry with flu antigens modulated by genetic components in the pathophysiology of T1N.
DOI: 10.1073/pnas.1818150116
PubMed: 30541895
Links to Exploration step
pubmed:30541895Le document en format XML
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mignot@stanford.edu.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="eISSN">1091-6490</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Autoantigens (metabolism)</term><term>Autoimmunity (immunology)</term><term>CD4-Positive T-Lymphocytes (immunology)</term><term>Child</term><term>Epitopes (immunology)</term><term>Female</term><term>HLA-DQ beta-Chains</term><term>Hemagglutinins</term><term>Humans</term><term>Influenza A Virus, H1N1 Subtype (immunology)</term><term>Influenza A virus (immunology)</term><term>Influenza A virus (pathogenicity)</term><term>Influenza, Human (immunology)</term><term>Intracellular Signaling Peptides and Proteins (genetics)</term><term>Male</term><term>Middle Aged</term><term>Molecular Mimicry (immunology)</term><term>Narcolepsy (immunology)</term><term>Orexins (genetics)</term><term>Orexins (immunology)</term><term>Orexins (metabolism)</term><term>Peptides (genetics)</term><term>Receptors, Antigen, T-Cell (genetics)</term><term>Vaccination</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Intracellular Signaling Peptides and Proteins</term><term>Orexins</term><term>Peptides</term><term>Receptors, Antigen, T-Cell</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Epitopes</term><term>Orexins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Autoantigens</term><term>Orexins</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Autoimmunity</term><term>CD4-Positive T-Lymphocytes</term><term>Influenza A Virus, H1N1 Subtype</term><term>Influenza A virus</term><term>Influenza, Human</term><term>Molecular Mimicry</term><term>Narcolepsy</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Influenza A virus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Child</term><term>Female</term><term>HLA-DQ beta-Chains</term><term>Hemagglutinins</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Vaccination</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Type 1 narcolepsy (T1N) is caused by hypocretin/orexin (HCRT) neuronal loss. Association with the HLA DQB1*06:02/DQA1*01:02 (98% vs. 25%) heterodimer (DQ0602), T cell receptors (TCR) and other immune loci suggest autoimmunity but autoantigens are unknown. Onset is seasonal and associated with influenza A, notably pandemic 2009 H1N1 (pH1N1) infection and vaccination (Pandemrix). Peptides derived from HCRT and influenza A, including pH1N1, were screened for DQ0602 binding and presence of cognate DQ0602 tetramer-peptide-specific CD4<sup>+</sup> T cells tested in 35 T1N cases and 22 DQ0602 controls. Higher reactivity to influenza pHA<sub>273-287</sub> (pH1N1 specific), PR8 (H1N1 pre-2009 and H2N2)-specific NP<sub>17-31</sub> and C-amidated but not native version of HCRT<sub>54-66</sub> and HCRT<sub>86-97</sub> (HCRT<sub>NH2</sub>) were observed in T1N. Single-cell TCR sequencing revealed sharing of CDR3β TRBV4-2-CASSQETQGRNYGYTF in HCRT<sub>NH2</sub> and pHA<sub>273-287</sub>-tetramers, suggesting molecular mimicry. This public CDR3β uses TRBV4-2, a segment modulated by T1N-associated SNP rs1008599, suggesting causality. TCR-α/β CDR3 motifs of HCRT<sub>54-66-NH2</sub> and HCRT<sub>86-97-NH2</sub> tetramers were extensively shared: notably public CDR3α, TRAV2-CAVETDSWGKLQF-TRAJ24, that uses TRAJ24, a chain modulated by T1N-associated SNPs rs1154155 and rs1483979. TCR-α/β CDR3 sequences found in pHA<sub>273-287</sub>, NP<sub>17-31</sub>, and HCRT<sub>NH2</sub> tetramer-positive CD4<sup>+</sup> cells were also retrieved in single INF-γ-secreting CD4<sup>+</sup> sorted cells stimulated with Pandemrix, independently confirming these results. Our results provide evidence for autoimmunity and molecular mimicry with flu antigens modulated by genetic components in the pathophysiology of T1N.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30541895</PMID><DateCompleted><Year>2019</Year><Month>03</Month><Day>22</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1091-6490</ISSN><JournalIssue CitedMedium="Internet"><Volume>115</Volume><Issue>52</Issue><PubDate><Year>2018</Year><Month>12</Month><Day>26</Day></PubDate></JournalIssue><Title>Proceedings of the National Academy of Sciences of the United States of America</Title><ISOAbbreviation>Proc. Natl. Acad. Sci. U.S.A.</ISOAbbreviation></Journal><ArticleTitle>Autoimmunity to hypocretin and molecular mimicry to flu in type 1 narcolepsy.</ArticleTitle><Pagination><MedlinePgn>E12323-E12332</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1073/pnas.1818150116</ELocationID><Abstract><AbstractText>Type 1 narcolepsy (T1N) is caused by hypocretin/orexin (HCRT) neuronal loss. Association with the HLA DQB1*06:02/DQA1*01:02 (98% vs. 25%) heterodimer (DQ0602), T cell receptors (TCR) and other immune loci suggest autoimmunity but autoantigens are unknown. Onset is seasonal and associated with influenza A, notably pandemic 2009 H1N1 (pH1N1) infection and vaccination (Pandemrix). Peptides derived from HCRT and influenza A, including pH1N1, were screened for DQ0602 binding and presence of cognate DQ0602 tetramer-peptide-specific CD4<sup>+</sup> T cells tested in 35 T1N cases and 22 DQ0602 controls. Higher reactivity to influenza pHA<sub>273-287</sub> (pH1N1 specific), PR8 (H1N1 pre-2009 and H2N2)-specific NP<sub>17-31</sub> and C-amidated but not native version of HCRT<sub>54-66</sub> and HCRT<sub>86-97</sub> (HCRT<sub>NH2</sub>) were observed in T1N. Single-cell TCR sequencing revealed sharing of CDR3β TRBV4-2-CASSQETQGRNYGYTF in HCRT<sub>NH2</sub> and pHA<sub>273-287</sub>-tetramers, suggesting molecular mimicry. This public CDR3β uses TRBV4-2, a segment modulated by T1N-associated SNP rs1008599, suggesting causality. TCR-α/β CDR3 motifs of HCRT<sub>54-66-NH2</sub> and HCRT<sub>86-97-NH2</sub> tetramers were extensively shared: notably public CDR3α, TRAV2-CAVETDSWGKLQF-TRAJ24, that uses TRAJ24, a chain modulated by T1N-associated SNPs rs1154155 and rs1483979. TCR-α/β CDR3 sequences found in pHA<sub>273-287</sub>, NP<sub>17-31</sub>, and HCRT<sub>NH2</sub> tetramer-positive CD4<sup>+</sup> cells were also retrieved in single INF-γ-secreting CD4<sup>+</sup> sorted cells stimulated with Pandemrix, independently confirming these results. Our results provide evidence for autoimmunity and molecular mimicry with flu antigens modulated by genetic components in the pathophysiology of T1N.</AbstractText><CopyrightInformation>Copyright © 2018 the Author(s). Published by PNAS.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Luo</LastName><ForeName>Guo</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Center for Sleep Sciences and Medicine, Stanford University School of Medicine, Palo Alto, CA 94304.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ambati</LastName><ForeName>Aditya</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Center for Sleep Sciences and Medicine, Stanford University School of Medicine, Palo Alto, CA 94304.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Ling</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Center for Sleep Sciences and Medicine, Stanford University School of Medicine, Palo Alto, CA 94304.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bonvalet</LastName><ForeName>Mélodie</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Center for Sleep Sciences and Medicine, Stanford University School of Medicine, Palo Alto, CA 94304.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Partinen</LastName><ForeName>Markku</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Helsinki Sleep Clinic, Vitalmed Research Centre, 00380 Helsinki, Finland.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical Neurosciences, University of Helsinki, 00100 Helsinki, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ji</LastName><ForeName>Xuhuai</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Immune Monitoring Center, Institute for Immunity, Transplantation, and Infection, Stanford University School of Medicine, Palo Alto, CA 94305.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maecker</LastName><ForeName>Holden Terry</ForeName><Initials>HT</Initials><AffiliationInfo><Affiliation>Immune Monitoring Center, Institute for Immunity, Transplantation, and Infection, Stanford University School of Medicine, Palo Alto, CA 94305.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mignot</LastName><ForeName>Emmanuel Jean-Marie</ForeName><Initials>EJ</Initials><AffiliationInfo><Affiliation>Center for Sleep Sciences and Medicine, Stanford University School of Medicine, Palo Alto, CA 94304; mignot@stanford.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HHSN272201300006C</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 NS023724</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>S10 OD020141</GrantID><Acronym>OD</Acronym><Agency>NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>12</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Proc Natl Acad Sci U S A</MedlineTA><NlmUniqueID>7505876</NlmUniqueID><ISSNLinking>0027-8424</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001324">Autoantigens</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000939">Epitopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C000596229">HCRT protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D059866">HLA-DQ beta-Chains</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C069051">HLA-DQB1 antigen</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006388">Hemagglutinins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D047908">Intracellular Signaling Peptides and Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000068797">Orexins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010455">Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011948">Receptors, Antigen, T-Cell</NameOfSubstance></Chemical></ChemicalList><SupplMeshList><SupplMeshName Type="Disease" UI="C563534">Narcolepsy 1</SupplMeshName></SupplMeshList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001324" MajorTopicYN="N">Autoantigens</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015551" MajorTopicYN="N">Autoimmunity</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015496" MajorTopicYN="N">CD4-Positive T-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000939" MajorTopicYN="N">Epitopes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059866" MajorTopicYN="N">HLA-DQ beta-Chains</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006388" MajorTopicYN="N">Hemagglutinins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053118" MajorTopicYN="N">Influenza A Virus, H1N1 Subtype</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009980" MajorTopicYN="N">Influenza A virus</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007251" MajorTopicYN="N">Influenza, Human</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D047908" MajorTopicYN="N">Intracellular Signaling Peptides and Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018716" MajorTopicYN="N">Molecular Mimicry</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009290" MajorTopicYN="N">Narcolepsy</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000068797" MajorTopicYN="N">Orexins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010455" MajorTopicYN="N">Peptides</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011948" MajorTopicYN="N">Receptors, Antigen, T-Cell</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014611" MajorTopicYN="N">Vaccination</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">DQ0602</Keyword><Keyword MajorTopicYN="Y">TCR</Keyword><Keyword MajorTopicYN="Y">autoimmunity</Keyword><Keyword MajorTopicYN="Y">narcolepsy</Keyword><Keyword MajorTopicYN="Y">tetramer</Keyword></KeywordList><CoiStatement>Conflict of interest statement: E.M. occasionally consults and has received contracts from Jazz Pharmaceuticals, is and has been a Principal Investigator on clinical trials using sodium oxybate and Solriamfetol, Jazz Pharmaceutical products, for the treatment of T1N; none of these have any scientific relationships to the study.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>12</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>3</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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