CBirTox is a selective antigen-specific agonist of the Treg-IgA-microbiota homeostatic pathway.
Identifieur interne : 000904 ( Main/Exploration ); précédent : 000903; suivant : 000905CBirTox is a selective antigen-specific agonist of the Treg-IgA-microbiota homeostatic pathway.
Auteurs : Katie L. Alexander [États-Unis] ; Jannet Katz [États-Unis] ; Charles O. Elson [États-Unis]Source :
- PloS one [ 1932-6203 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Cellules dendritiques (immunologie), Cellules présentatrices d'antigène (métabolisme), Facteur de croissance transformant bêta (métabolisme), Facteurs de transcription Forkhead (métabolisme), Flagelline (agonistes), Génomique (MeSH), Homéostasie (MeSH), Immunoglobuline A (immunologie), Intestins (MeSH), Lignée cellulaire (MeSH), Lymphocytes B (immunologie), Lymphocytes T régulateurs (immunologie), Microbiote (MeSH), Protéines de fusion recombinantes (métabolisme), Souris de lignée C57BL (MeSH), Sérine-thréonine kinases TOR (métabolisme), Toxine cholérique (métabolisme), Transduction du signal (MeSH), Trétinoïne (métabolisme), Épitopes (immunologie).
- MESH :
- agonistes : Flagelline.
- immunologie : Cellules dendritiques, Immunoglobuline A, Lymphocytes B, Lymphocytes T régulateurs, Épitopes.
- métabolisme : Cellules présentatrices d'antigène, Facteur de croissance transformant bêta, Facteurs de transcription Forkhead, Protéines de fusion recombinantes, Sérine-thréonine kinases TOR, Toxine cholérique, Trétinoïne.
- Animaux, Génomique, Homéostasie, Intestins, Lignée cellulaire, Microbiote, Souris de lignée C57BL, Transduction du signal.
English descriptors
- KwdEn :
- Animals (MeSH), Antigen-Presenting Cells (metabolism), B-Lymphocytes (immunology), Cell Line (MeSH), Cholera Toxin (metabolism), Dendritic Cells (immunology), Epitopes (immunology), Flagellin (agonists), Forkhead Transcription Factors (metabolism), Genomics (MeSH), Homeostasis (MeSH), Immunoglobulin A (immunology), Intestines (MeSH), Mice, Inbred C57BL (MeSH), Microbiota (MeSH), Recombinant Fusion Proteins (metabolism), Signal Transduction (MeSH), T-Lymphocytes, Regulatory (immunology), TOR Serine-Threonine Kinases (metabolism), Transforming Growth Factor beta (metabolism), Tretinoin (metabolism).
- MESH :
- chemical , agonists : Flagellin.
- chemical , immunology : Epitopes, Immunoglobulin A.
- chemical , metabolism : Cholera Toxin, Forkhead Transcription Factors, Recombinant Fusion Proteins, TOR Serine-Threonine Kinases, Transforming Growth Factor beta, Tretinoin.
- immunology : B-Lymphocytes, Dendritic Cells, T-Lymphocytes, Regulatory.
- metabolism : Antigen-Presenting Cells.
- Animals, Cell Line, Genomics, Homeostasis, Intestines, Mice, Inbred C57BL, Microbiota, Signal Transduction.
Abstract
Cultivating an environment of mutualism between host cells and the microbiota is vital, and dysregulation of this relationship is associated with multiple immune disorders including metabolic and skin diseases, asthma, allergy, and Inflammatory Bowel Disease (IBD). One prominent mechanism for maintaining homeostasis is the protective regulatory T cell (Treg)- Immunoglobulin A (IgA) pathway toward microbiota antigens, in which Tregs maintain homeostasis and provide critical survival factors to IgA+ B cells. In order to amplify the Treg-IgA pathway, we have generated a fusion protein, CBirTox, comprised of a portion of the carboxy terminus of CBir1, a microbiota flagellin, genetically coupled to Cholera Toxin B subunit (CTB) via the A2 linker of CT. Both dendritic cells (DCs) and B cells pulsed with CBirTox selectively induced functional CD4+Foxp3+ Tregs in vitro, and CBirTox augmented CD4+Foxp3+ cell numbers in vivo. The induced Foxp3 expression was independent of retinoic acid (RA) signaling but was inhibited by neutralization of TGF-β. CBirTox treatment of B cells downregulated mammalian target of rapamycin (mTOR) signaling. Furthermore, CBirTox-pulsed DCs induced substantial production of IgA from naïve B cells. Collectively these data demonstrate that CBirTox represents a novel approach to bolstering the Treg-IgA pathway at the host-microbiota interface.
DOI: 10.1371/journal.pone.0181866
PubMed: 28750075
PubMed Central: PMC5531474
Affiliations:
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signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cultivating an environment of mutualism between host cells and the microbiota is vital, and dysregulation of this relationship is associated with multiple immune disorders including metabolic and skin diseases, asthma, allergy, and Inflammatory Bowel Disease (IBD). One prominent mechanism for maintaining homeostasis is the protective regulatory T cell (Treg)- Immunoglobulin A (IgA) pathway toward microbiota antigens, in which Tregs maintain homeostasis and provide critical survival factors to IgA+ B cells. In order to amplify the Treg-IgA pathway, we have generated a fusion protein, CBirTox, comprised of a portion of the carboxy terminus of CBir1, a microbiota flagellin, genetically coupled to Cholera Toxin B subunit (CTB) via the A2 linker of CT. Both dendritic cells (DCs) and B cells pulsed with CBirTox selectively induced functional CD4+Foxp3+ Tregs in vitro, and CBirTox augmented CD4+Foxp3+ cell numbers in vivo. The induced Foxp3 expression was independent of retinoic acid (RA) signaling but was inhibited by neutralization of TGF-β. CBirTox treatment of B cells downregulated mammalian target of rapamycin (mTOR) signaling. Furthermore, CBirTox-pulsed DCs induced substantial production of IgA from naïve B cells. Collectively these data demonstrate that CBirTox represents a novel approach to bolstering the Treg-IgA pathway at the host-microbiota interface.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28750075</PMID><DateCompleted><Year>2017</Year><Month>10</Month><Day>09</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>12</Volume><Issue>7</Issue><PubDate><Year>2017</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS One</ISOAbbreviation></Journal><ArticleTitle>CBirTox is a selective antigen-specific agonist of the Treg-IgA-microbiota homeostatic pathway.</ArticleTitle><Pagination><MedlinePgn>e0181866</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0181866</ELocationID><Abstract><AbstractText>Cultivating an environment of mutualism between host cells and the microbiota is vital, and dysregulation of this relationship is associated with multiple immune disorders including metabolic and skin diseases, asthma, allergy, and Inflammatory Bowel Disease (IBD). One prominent mechanism for maintaining homeostasis is the protective regulatory T cell (Treg)- Immunoglobulin A (IgA) pathway toward microbiota antigens, in which Tregs maintain homeostasis and provide critical survival factors to IgA+ B cells. In order to amplify the Treg-IgA pathway, we have generated a fusion protein, CBirTox, comprised of a portion of the carboxy terminus of CBir1, a microbiota flagellin, genetically coupled to Cholera Toxin B subunit (CTB) via the A2 linker of CT. Both dendritic cells (DCs) and B cells pulsed with CBirTox selectively induced functional CD4+Foxp3+ Tregs in vitro, and CBirTox augmented CD4+Foxp3+ cell numbers in vivo. The induced Foxp3 expression was independent of retinoic acid (RA) signaling but was inhibited by neutralization of TGF-β. CBirTox treatment of B cells downregulated mammalian target of rapamycin (mTOR) signaling. Furthermore, CBirTox-pulsed DCs induced substantial production of IgA from naïve B cells. Collectively these data demonstrate that CBirTox represents a novel approach to bolstering the Treg-IgA pathway at the host-microbiota interface.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Alexander</LastName><ForeName>Katie L</ForeName><Initials>KL</Initials><AffiliationInfo><Affiliation>Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Katz</LastName><ForeName>Jannet</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pediatric Dentistry, University of Alabama at Birmingham, Birmingham, AL, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Elson</LastName><ForeName>Charles O</ForeName><Initials>CO</Initials><Identifier Source="ORCID">http://orcid.org/0000-0001-8873-1534</Identifier><AffiliationInfo><Affiliation>Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States of America.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL, United States of America.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>07</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C502160">CBir1 flagellin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000939">Epitopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000938" MajorTopicYN="N">Antigen-Presenting Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001402" MajorTopicYN="N">B-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002772" MajorTopicYN="N">Cholera Toxin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003713" MajorTopicYN="N">Dendritic Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000939" MajorTopicYN="N">Epitopes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005408" MajorTopicYN="N">Flagellin</DescriptorName><QualifierName UI="Q000819" MajorTopicYN="Y">agonists</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051858" MajorTopicYN="N">Forkhead Transcription Factors</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D023281" MajorTopicYN="N">Genomics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006706" MajorTopicYN="Y">Homeostasis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007070" MajorTopicYN="N">Immunoglobulin A</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007422" MajorTopicYN="N">Intestines</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D064307" MajorTopicYN="Y">Microbiota</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011993" MajorTopicYN="N">Recombinant Fusion Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050378" MajorTopicYN="N">T-Lymphocytes, Regulatory</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000378" 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Alexander</name></region><name sortKey="Elson, Charles O" sort="Elson, Charles O" uniqKey="Elson C" first="Charles O" last="Elson">Charles O. Elson</name><name sortKey="Elson, Charles O" sort="Elson, Charles O" uniqKey="Elson C" first="Charles O" last="Elson">Charles O. Elson</name><name sortKey="Katz, Jannet" sort="Katz, Jannet" uniqKey="Katz J" first="Jannet" last="Katz">Jannet Katz</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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