The L3 of Brugia induces a Th2-polarized response following activation of an IL-4-producing CD4-CD8- alphabeta T cell population.
Identifieur interne : 00BD06 ( Ncbi/Merge ); précédent : 00BD05; suivant : 00BD07The L3 of Brugia induces a Th2-polarized response following activation of an IL-4-producing CD4-CD8- alphabeta T cell population.
Auteurs : J. Osborne [Royaume-Uni] ; E. DevaneySource :
- International immunology [ 0953-8178 ] ; 1998.
Descripteurs français
- KwdFr :
- ARN messager (biosynthèse), Activation des lymphocytes, Animaux, Brugia (immunologie), Cytokines (génétique), Facteurs temps, Filariose lymphatique (métabolisme), Interleukine-10 (génétique), Interleukine-2 (génétique), Interleukine-4 (biosynthèse), Interleukine-4 (génétique), Larve (immunologie), Lymphocytes T (immunologie), Lymphocytes T (métabolisme), Lymphocytes T (physiologie), Lymphocytes T CD4+ (métabolisme), Lymphocytes T CD8+ (métabolisme), Lymphocytes auxiliaires Th2 (immunologie), Microfilaria (immunologie), Mâle, Récepteur lymphocytaire T antigène, alpha-bêta (biosynthèse), Récepteur lymphocytaire T antigène, gamma-delta (biosynthèse), Souris, Souris de lignée BALB C.
- MESH :
- biosynthèse : ARN messager, Interleukine-4, Récepteur lymphocytaire T antigène, alpha-bêta, Récepteur lymphocytaire T antigène, gamma-delta.
- génétique : Cytokines, Interleukine-10, Interleukine-2, Interleukine-4.
- immunologie : Brugia, Larve, Lymphocytes T, Lymphocytes auxiliaires Th2, Microfilaria.
- métabolisme : Filariose lymphatique, Lymphocytes T, Lymphocytes T CD4+, Lymphocytes T CD8+.
- physiologie : Lymphocytes T.
- Activation des lymphocytes, Animaux, Facteurs temps, Mâle, Souris, Souris de lignée BALB C.
English descriptors
- KwdEn :
- Animals, Brugia (immunology), CD4-Positive T-Lymphocytes (metabolism), CD8-Positive T-Lymphocytes (metabolism), Cytokines (genetics), Elephantiasis, Filarial (metabolism), Interleukin-10 (genetics), Interleukin-2 (genetics), Interleukin-4 (biosynthesis), Interleukin-4 (genetics), Larva (immunology), Lymphocyte Activation, Male, Mice, Mice, Inbred BALB C, Microfilariae (immunology), RNA, Messenger (biosynthesis), Receptors, Antigen, T-Cell, alpha-beta (biosynthesis), Receptors, Antigen, T-Cell, gamma-delta (biosynthesis), T-Lymphocytes (immunology), T-Lymphocytes (metabolism), T-Lymphocytes (physiology), Th2 Cells (immunology), Time Factors.
- MESH :
- chemical , biosynthesis : Interleukin-4, RNA, Messenger, Receptors, Antigen, T-Cell, alpha-beta, Receptors, Antigen, T-Cell, gamma-delta.
- chemical , genetics : Cytokines, Interleukin-10, Interleukin-2, Interleukin-4.
- immunology : Brugia, Larva, Microfilariae, T-Lymphocytes, Th2 Cells.
- metabolism : CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Elephantiasis, Filarial, T-Lymphocytes.
- physiology : T-Lymphocytes.
- Animals, Lymphocyte Activation, Male, Mice, Mice, Inbred BALB C, Time Factors.
Abstract
Lymphatic filariasis in man is characterized by a profound bias in the immune response. Parasite-specific Th1 responses are dramatically down-regulated while Th2 responses dominate. We have used the infective larval stage of the nematode parasite Brugia pahangi, a potent Th2 inducer in naive mice, to examine cytokine production during the initiation phase of the response. For comparative purposes, the early cytokine transcription pattern elicited by microfilariae (mf), another life cycle stage of the parasite known to induce a primary Th1 response, was analysed in parallel. At 24 h post-infection (p.i.) a burst of IL-4 transcription was detected in the draining popliteal lymph node of L3-infected animals. IL-4 was the only cytokine transcript detectable at this early time point and was not present in mf-infected mice. From day 4 p.i. onwards, the L3 elicited a Th2 response as defined at the level of cytokine mRNA and protein production by CD4+ cells. In contrast, mf stimulate high levels of IFN-gamma mRNA at day 4 p.i. in the absence of IL-4 or IL-10 induction. Cell selection analysis indicated that IL-4 produced at 24 h derived from a population of CD4-CD8- alphabeta T cells. These results suggest that triggering of an unusual double-negative T cell population to secrete IL-4 at the very outset of infection with the L3 of B. pahangi may be the critical factor favouring the development of antigen-specific Th2 cells in response to this stage of the parasite.
PubMed: 9796925
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pubmed:9796925Le document en format XML
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Parasite-specific Th1 responses are dramatically down-regulated while Th2 responses dominate. We have used the infective larval stage of the nematode parasite Brugia pahangi, a potent Th2 inducer in naive mice, to examine cytokine production during the initiation phase of the response. For comparative purposes, the early cytokine transcription pattern elicited by microfilariae (mf), another life cycle stage of the parasite known to induce a primary Th1 response, was analysed in parallel. At 24 h post-infection (p.i.) a burst of IL-4 transcription was detected in the draining popliteal lymph node of L3-infected animals. IL-4 was the only cytokine transcript detectable at this early time point and was not present in mf-infected mice. From day 4 p.i. onwards, the L3 elicited a Th2 response as defined at the level of cytokine mRNA and protein production by CD4+ cells. In contrast, mf stimulate high levels of IFN-gamma mRNA at day 4 p.i. in the absence of IL-4 or IL-10 induction. Cell selection analysis indicated that IL-4 produced at 24 h derived from a population of CD4-CD8- alphabeta T cells. These results suggest that triggering of an unusual double-negative T cell population to secrete IL-4 at the very outset of infection with the L3 of B. pahangi may be the critical factor favouring the development of antigen-specific Th2 cells in response to this stage of the parasite.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9796925</PMID><DateCreated><Year>1999</Year><Month>02</Month><Day>03</Day></DateCreated><DateCompleted><Year>1999</Year><Month>02</Month><Day>03</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0953-8178</ISSN><JournalIssue CitedMedium="Print"><Volume>10</Volume><Issue>10</Issue><PubDate><Year>1998</Year><Month>Oct</Month></PubDate></JournalIssue><Title>International immunology</Title><ISOAbbreviation>Int. Immunol.</ISOAbbreviation></Journal><ArticleTitle>The L3 of Brugia induces a Th2-polarized response following activation of an IL-4-producing CD4-CD8- alphabeta T cell population.</ArticleTitle><Pagination><MedlinePgn>1583-90</MedlinePgn></Pagination><Abstract><AbstractText>Lymphatic filariasis in man is characterized by a profound bias in the immune response. Parasite-specific Th1 responses are dramatically down-regulated while Th2 responses dominate. We have used the infective larval stage of the nematode parasite Brugia pahangi, a potent Th2 inducer in naive mice, to examine cytokine production during the initiation phase of the response. For comparative purposes, the early cytokine transcription pattern elicited by microfilariae (mf), another life cycle stage of the parasite known to induce a primary Th1 response, was analysed in parallel. At 24 h post-infection (p.i.) a burst of IL-4 transcription was detected in the draining popliteal lymph node of L3-infected animals. IL-4 was the only cytokine transcript detectable at this early time point and was not present in mf-infected mice. From day 4 p.i. onwards, the L3 elicited a Th2 response as defined at the level of cytokine mRNA and protein production by CD4+ cells. In contrast, mf stimulate high levels of IFN-gamma mRNA at day 4 p.i. in the absence of IL-4 or IL-10 induction. Cell selection analysis indicated that IL-4 produced at 24 h derived from a population of CD4-CD8- alphabeta T cells. These results suggest that triggering of an unusual double-negative T cell population to secrete IL-4 at the very outset of infection with the L3 of B. pahangi may be the critical factor favouring the development of antigen-specific Th2 cells in response to this stage of the parasite.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Osborne</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Veterinary Parasitology, University of Glasgow, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Devaney</LastName><ForeName>E</ForeName><Initials>E</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Int Immunol</MedlineTA><NlmUniqueID>8916182</NlmUniqueID><ISSNLinking>0953-8178</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007376">Interleukin-2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016693">Receptors, Antigen, T-Cell, alpha-beta</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016692">Receptors, Antigen, T-Cell, gamma-delta</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>IM</CitationSubset><CitationSubset>X</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002009" MajorTopicYN="N">Brugia</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015496" MajorTopicYN="N">CD4-Positive T-Lymphocytes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018414" MajorTopicYN="N">CD8-Positive T-Lymphocytes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004605" MajorTopicYN="N">Elephantiasis, Filarial</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016753" MajorTopicYN="N">Interleukin-10</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007376" MajorTopicYN="N">Interleukin-2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015847" MajorTopicYN="N">Interleukin-4</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007814" MajorTopicYN="N">Larva</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008213" MajorTopicYN="N">Lymphocyte Activation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008842" MajorTopicYN="N">Microfilariae</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016693" MajorTopicYN="N">Receptors, Antigen, T-Cell, alpha-beta</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016692" MajorTopicYN="N">Receptors, Antigen, T-Cell, gamma-delta</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013601" MajorTopicYN="N">T-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018418" MajorTopicYN="N">Th2 Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1998</Year><Month>10</Month><Day>31</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1998</Year><Month>10</Month><Day>31</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1998</Year><Month>10</Month><Day>31</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9796925</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Écosse</li></region><settlement><li>Glasgow</li></settlement><orgName><li>Université de Glasgow</li></orgName></list><tree><noCountry><name sortKey="Devaney, E" sort="Devaney, E" uniqKey="Devaney E" first="E" last="Devaney">E. Devaney</name></noCountry><country name="Royaume-Uni"><region name="Écosse"><name sortKey="Osborne, J" sort="Osborne, J" uniqKey="Osborne J" first="J" last="Osborne">J. Osborne</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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