IL-4-, TGF-β-, and IL-1-dependent expansion of parasite antigen-specific Th9 cells is associated with clinical pathology in human lymphatic filariasis.
Identifieur interne : 001986 ( PubMed/Curation ); précédent : 001985; suivant : 001987IL-4-, TGF-β-, and IL-1-dependent expansion of parasite antigen-specific Th9 cells is associated with clinical pathology in human lymphatic filariasis.
Auteurs : Rajamanickam Anuradha [Inde] ; Parakkal Jovvian George ; Luke E. Hanna ; Vedachalam Chandrasekaran ; Paul Kumaran ; Thomas B. Nutman ; Subash BabuSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2013.
Descripteurs français
- KwdFr :
- Facteur de croissance transformant bêta (immunologie), Facteur de croissance transformant bêta (métabolisme), Filariose lymphatique (immunologie), Filariose lymphatique (métabolisme), Humains, Interleukine-1 (immunologie), Interleukine-1 (métabolisme), Interleukine-10 (biosynthèse), Interleukine-10 (immunologie), Interleukine-4 (immunologie), Interleukine-4 (métabolisme), Interleukine-9 (biosynthèse), Interleukine-9 (immunologie), Lymphocytes T CD4+ (immunologie), Lymphocytes T CD4+ (métabolisme), Sous-populations de lymphocytes T (immunologie), Sous-populations de lymphocytes T (métabolisme), Test ELISA.
- MESH :
- biosynthèse : Interleukine-10, Interleukine-9.
- immunologie : Facteur de croissance transformant bêta, Filariose lymphatique, Interleukine-1, Interleukine-10, Interleukine-4, Interleukine-9, Lymphocytes T CD4+, Sous-populations de lymphocytes T.
- métabolisme : Facteur de croissance transformant bêta, Filariose lymphatique, Interleukine-1, Interleukine-4, Lymphocytes T CD4+, Sous-populations de lymphocytes T.
- Humains, Test ELISA.
English descriptors
- KwdEn :
- CD4-Positive T-Lymphocytes (immunology), CD4-Positive T-Lymphocytes (metabolism), Elephantiasis, Filarial (immunology), Elephantiasis, Filarial (metabolism), Enzyme-Linked Immunosorbent Assay, Humans, Interleukin-1 (immunology), Interleukin-1 (metabolism), Interleukin-10 (biosynthesis), Interleukin-10 (immunology), Interleukin-4 (immunology), Interleukin-4 (metabolism), Interleukin-9 (biosynthesis), Interleukin-9 (immunology), T-Lymphocyte Subsets (immunology), T-Lymphocyte Subsets (metabolism), Transforming Growth Factor beta (immunology), Transforming Growth Factor beta (metabolism).
- MESH :
- chemical , biosynthesis : Interleukin-10, Interleukin-9.
- chemical , immunology : Interleukin-1, Interleukin-10, Interleukin-4, Interleukin-9, Transforming Growth Factor beta.
- immunology : CD4-Positive T-Lymphocytes, Elephantiasis, Filarial, T-Lymphocyte Subsets.
- metabolism : CD4-Positive T-Lymphocytes, Elephantiasis, Filarial, Interleukin-1, Interleukin-4, T-Lymphocyte Subsets, Transforming Growth Factor beta.
- Enzyme-Linked Immunosorbent Assay, Humans.
Abstract
Th9 cells are a subset of CD4(+) T cells, shown to be important in allergy, autoimmunity, and antitumor responses; however, their role in human infectious diseases has not been explored in detail. We identified a population of IL-9 and IL-10 coexpressing cells (lacking IL-4 expression) in normal individuals. These cells respond to antigenic and mitogenic stimulation, but are distinct from IL-9(+) Th2 cells. We also demonstrate that these Th9 cells exhibit Ag-specific expansion in a chronic helminth infection (lymphatic filariasis). Comparison of Th9 responses reveals that individuals with pathology associated with filarial infection exhibit significantly expanded frequencies of filarial Ag-induced Th9 cells, but not of IL9(+)Th2 cells in comparison with filarial-infected individuals without associated disease. Moreover, the per cell production of IL-9 is significantly higher in Th9 cells compared with IL9(+)Th2 cells, indicating that the Th9 cells are the predominant CD4(+) T cell subset producing IL-9 in the context of human infection. This expansion was reflected in elevated Ag-stimulated IL-9 cytokine levels in whole blood culture supernatants. Finally, the frequencies of Th9 cells correlated positively with the severity of lymphedema (and presumed inflammation) in filarial-diseased individuals. This expansion of Th9 cells was dependent on IL-4, TGF-β, and IL-1 in vitro. We have therefore identified an important human CD4(+) T cell subpopulation coexpressing IL-9 and IL-10, but not IL-4, the expansion of which is associated with disease in chronic lymphatic filariasis and could potentially have an important role in the pathogenesis of other inflammatory disorders.
DOI: 10.4049/jimmunol.1300911
PubMed: 23913964
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pubmed:23913964Le document en format XML
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Hanna</name></author><author><name sortKey="Chandrasekaran, Vedachalam" sort="Chandrasekaran, Vedachalam" uniqKey="Chandrasekaran V" first="Vedachalam" last="Chandrasekaran">Vedachalam Chandrasekaran</name></author><author><name sortKey="Kumaran, Paul" sort="Kumaran, Paul" uniqKey="Kumaran P" first="Paul" last="Kumaran">Paul Kumaran</name></author><author><name sortKey="Nutman, Thomas B" sort="Nutman, Thomas B" uniqKey="Nutman T" first="Thomas B" last="Nutman">Thomas B. 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Hanna</name></author><author><name sortKey="Chandrasekaran, Vedachalam" sort="Chandrasekaran, Vedachalam" uniqKey="Chandrasekaran V" first="Vedachalam" last="Chandrasekaran">Vedachalam Chandrasekaran</name></author><author><name sortKey="Kumaran, Paul" sort="Kumaran, Paul" uniqKey="Kumaran P" first="Paul" last="Kumaran">Paul Kumaran</name></author><author><name sortKey="Nutman, Thomas B" sort="Nutman, Thomas B" uniqKey="Nutman T" first="Thomas B" last="Nutman">Thomas B. 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We identified a population of IL-9 and IL-10 coexpressing cells (lacking IL-4 expression) in normal individuals. These cells respond to antigenic and mitogenic stimulation, but are distinct from IL-9(+) Th2 cells. We also demonstrate that these Th9 cells exhibit Ag-specific expansion in a chronic helminth infection (lymphatic filariasis). Comparison of Th9 responses reveals that individuals with pathology associated with filarial infection exhibit significantly expanded frequencies of filarial Ag-induced Th9 cells, but not of IL9(+)Th2 cells in comparison with filarial-infected individuals without associated disease. Moreover, the per cell production of IL-9 is significantly higher in Th9 cells compared with IL9(+)Th2 cells, indicating that the Th9 cells are the predominant CD4(+) T cell subset producing IL-9 in the context of human infection. This expansion was reflected in elevated Ag-stimulated IL-9 cytokine levels in whole blood culture supernatants. Finally, the frequencies of Th9 cells correlated positively with the severity of lymphedema (and presumed inflammation) in filarial-diseased individuals. This expansion of Th9 cells was dependent on IL-4, TGF-β, and IL-1 in vitro. We have therefore identified an important human CD4(+) T cell subpopulation coexpressing IL-9 and IL-10, but not IL-4, the expansion of which is associated with disease in chronic lymphatic filariasis and could potentially have an important role in the pathogenesis of other inflammatory disorders.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23913964</PMID><DateCreated><Year>2013</Year><Month>08</Month><Day>21</Day></DateCreated><DateCompleted><Year>2013</Year><Month>11</Month><Day>06</Day></DateCompleted><DateRevised><Year>2016</Year><Month>12</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1550-6606</ISSN><JournalIssue CitedMedium="Internet"><Volume>191</Volume><Issue>5</Issue><PubDate><Year>2013</Year><Month>Sep</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J. Immunol.</ISOAbbreviation></Journal><ArticleTitle>IL-4-, TGF-β-, and IL-1-dependent expansion of parasite antigen-specific Th9 cells is associated with clinical pathology in human lymphatic filariasis.</ArticleTitle><Pagination><MedlinePgn>2466-73</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4049/jimmunol.1300911</ELocationID><Abstract><AbstractText>Th9 cells are a subset of CD4(+) T cells, shown to be important in allergy, autoimmunity, and antitumor responses; however, their role in human infectious diseases has not been explored in detail. We identified a population of IL-9 and IL-10 coexpressing cells (lacking IL-4 expression) in normal individuals. These cells respond to antigenic and mitogenic stimulation, but are distinct from IL-9(+) Th2 cells. We also demonstrate that these Th9 cells exhibit Ag-specific expansion in a chronic helminth infection (lymphatic filariasis). Comparison of Th9 responses reveals that individuals with pathology associated with filarial infection exhibit significantly expanded frequencies of filarial Ag-induced Th9 cells, but not of IL9(+)Th2 cells in comparison with filarial-infected individuals without associated disease. Moreover, the per cell production of IL-9 is significantly higher in Th9 cells compared with IL9(+)Th2 cells, indicating that the Th9 cells are the predominant CD4(+) T cell subset producing IL-9 in the context of human infection. This expansion was reflected in elevated Ag-stimulated IL-9 cytokine levels in whole blood culture supernatants. Finally, the frequencies of Th9 cells correlated positively with the severity of lymphedema (and presumed inflammation) in filarial-diseased individuals. This expansion of Th9 cells was dependent on IL-4, TGF-β, and IL-1 in vitro. We have therefore identified an important human CD4(+) T cell subpopulation coexpressing IL-9 and IL-10, but not IL-4, the expansion of which is associated with disease in chronic lymphatic filariasis and could potentially have an important role in the pathogenesis of other inflammatory disorders.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Anuradha</LastName><ForeName>Rajamanickam</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>National Institutes of Health-International Center for Excellence in Research, Chennai 600031, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>George</LastName><ForeName>Parakkal Jovvian</ForeName><Initials>PJ</Initials></Author><Author ValidYN="Y"><LastName>Hanna</LastName><ForeName>Luke E</ForeName><Initials>LE</Initials></Author><Author ValidYN="Y"><LastName>Chandrasekaran</LastName><ForeName>Vedachalam</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Kumaran</LastName><ForeName>Paul</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Nutman</LastName><ForeName>Thomas B</ForeName><Initials>TB</Initials></Author><Author ValidYN="Y"><LastName>Babu</LastName><ForeName>Subash</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>Z99 AI999999</GrantID><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>08</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Immunol</MedlineTA><NlmUniqueID>2985117R</NlmUniqueID><ISSNLinking>0022-1767</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C508598">IL4 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007375">Interleukin-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016906">Interleukin-9</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016212">Transforming Growth Factor beta</NameOfSubstance></Chemical><Chemical><RegistryNumber>130068-27-8</RegistryNumber><NameOfSubstance UI="D016753">Interleukin-10</NameOfSubstance></Chemical><Chemical><RegistryNumber>207137-56-2</RegistryNumber><NameOfSubstance UI="D015847">Interleukin-4</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections 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