T cells facilitate Brugia malayi development in TCRalpha(null) mice.
Identifieur interne : 004C15 ( PubMed/Corpus ); précédent : 004C14; suivant : 004C16T cells facilitate Brugia malayi development in TCRalpha(null) mice.
Auteurs : S. Babu ; L D Shultz ; T V RajanSource :
- Experimental parasitology [ 0014-4894 ] ; 1999.
English descriptors
- KwdEn :
- Animals, Brugia malayi (growth & development), Brugia malayi (immunology), Elephantiasis, Filarial (immunology), Elephantiasis, Filarial (parasitology), Host-Parasite Interactions, Immunocompetence, Immunocompromised Host, Mice, Mice, Inbred C57BL, Mice, SCID, Phenotype, Receptors, Antigen, T-Cell, alpha-beta (genetics), Receptors, Antigen, T-Cell, alpha-beta (immunology), T-Lymphocytes (immunology), T-Lymphocytes (physiology).
- MESH :
- chemical , genetics : Receptors, Antigen, T-Cell, alpha-beta.
- growth & development : Brugia malayi.
- immunology : Brugia malayi, Elephantiasis, Filarial, Receptors, Antigen, T-Cell, alpha-beta, T-Lymphocytes.
- parasitology : Elephantiasis, Filarial.
- physiology : T-Lymphocytes.
- Animals, Host-Parasite Interactions, Immunocompetence, Immunocompromised Host, Mice, Mice, Inbred C57BL, Mice, SCID, Phenotype.
Abstract
The host-parasite interactions of Brugia malayi in mice are complex and multifactorial. In order to study the role of T cells in early B. malayi development, we infected TCRalpha(null) mice, which retain a population of CD4+ TCRbeta+ cells and TCRbeta(null) mice, which lack all TCRalphabeta(+) T cells. TCRalpha(null) mice were permissive to L4 larval and adult worm development but TCRbeta(null) mice were not. Depletion of the CD4(+) T cells in the former abrogated the permissive phenotype. It appears that the CD4(+) TCRbeta(+) T cells that have been described in TCRalpha(null) mice may facilitate early B. malayi development. These data are similar to our earlier demonstration of the role of NK cells in facilitating worm growth in SCID mice.
DOI: 10.1006/expr.1999.4438
PubMed: 10464039
Links to Exploration step
pubmed:10464039Le document en format XML
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Babu</name><affiliation><nlm:affiliation>Department of Pathology, University of Connecticut Health Center, Connecticut, Farmington 06030, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Shultz, L D" sort="Shultz, L D" uniqKey="Shultz L" first="L D" last="Shultz">L D Shultz</name></author><author><name sortKey="Rajan, T V" sort="Rajan, T V" uniqKey="Rajan T" first="T V" last="Rajan">T V Rajan</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1999">1999</date><idno type="RBID">pubmed:10464039</idno><idno type="pmid">10464039</idno><idno type="doi">10.1006/expr.1999.4438</idno><idno type="wicri:Area/PubMed/Corpus">004C15</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">004C15</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">T cells facilitate Brugia malayi development in TCRalpha(null) mice.</title><author><name sortKey="Babu, S" sort="Babu, S" uniqKey="Babu S" first="S" last="Babu">S. Babu</name><affiliation><nlm:affiliation>Department of Pathology, University of Connecticut Health Center, Connecticut, Farmington 06030, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Shultz, L D" sort="Shultz, L D" uniqKey="Shultz L" first="L D" last="Shultz">L D Shultz</name></author><author><name sortKey="Rajan, T V" sort="Rajan, T V" uniqKey="Rajan T" first="T V" last="Rajan">T V Rajan</name></author></analytic><series><title level="j">Experimental parasitology</title><idno type="ISSN">0014-4894</idno><imprint><date when="1999" type="published">1999</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Brugia malayi (growth & development)</term><term>Brugia malayi (immunology)</term><term>Elephantiasis, Filarial (immunology)</term><term>Elephantiasis, Filarial (parasitology)</term><term>Host-Parasite Interactions</term><term>Immunocompetence</term><term>Immunocompromised Host</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, SCID</term><term>Phenotype</term><term>Receptors, Antigen, T-Cell, alpha-beta (genetics)</term><term>Receptors, Antigen, T-Cell, alpha-beta (immunology)</term><term>T-Lymphocytes (immunology)</term><term>T-Lymphocytes (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptors, Antigen, T-Cell, alpha-beta</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Brugia malayi</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Brugia malayi</term><term>Elephantiasis, Filarial</term><term>Receptors, Antigen, T-Cell, alpha-beta</term><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="parasitology" xml:lang="en"><term>Elephantiasis, Filarial</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Host-Parasite Interactions</term><term>Immunocompetence</term><term>Immunocompromised Host</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, SCID</term><term>Phenotype</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The host-parasite interactions of Brugia malayi in mice are complex and multifactorial. In order to study the role of T cells in early B. malayi development, we infected TCRalpha(null) mice, which retain a population of CD4+ TCRbeta+ cells and TCRbeta(null) mice, which lack all TCRalphabeta(+) T cells. TCRalpha(null) mice were permissive to L4 larval and adult worm development but TCRbeta(null) mice were not. Depletion of the CD4(+) T cells in the former abrogated the permissive phenotype. It appears that the CD4(+) TCRbeta(+) T cells that have been described in TCRalpha(null) mice may facilitate early B. malayi development. These data are similar to our earlier demonstration of the role of NK cells in facilitating worm growth in SCID mice.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10464039</PMID><DateCreated><Year>1999</Year><Month>09</Month><Day>09</Day></DateCreated><DateCompleted><Year>1999</Year><Month>09</Month><Day>09</Day></DateCompleted><DateRevised><Year>2007</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0014-4894</ISSN><JournalIssue CitedMedium="Print"><Volume>93</Volume><Issue>1</Issue><PubDate><Year>1999</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Experimental parasitology</Title><ISOAbbreviation>Exp. Parasitol.</ISOAbbreviation></Journal><ArticleTitle>T cells facilitate Brugia malayi development in TCRalpha(null) mice.</ArticleTitle><Pagination><MedlinePgn>55-7</MedlinePgn></Pagination><Abstract><AbstractText>The host-parasite interactions of Brugia malayi in mice are complex and multifactorial. In order to study the role of T cells in early B. malayi development, we infected TCRalpha(null) mice, which retain a population of CD4+ TCRbeta+ cells and TCRbeta(null) mice, which lack all TCRalphabeta(+) T cells. TCRalpha(null) mice were permissive to L4 larval and adult worm development but TCRbeta(null) mice were not. Depletion of the CD4(+) T cells in the former abrogated the permissive phenotype. It appears that the CD4(+) TCRbeta(+) T cells that have been described in TCRalpha(null) mice may facilitate early B. malayi development. These data are similar to our earlier demonstration of the role of NK cells in facilitating worm growth in SCID mice.</AbstractText><CopyrightInformation>Copyright 1999 Academic Press.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Babu</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Connecticut Health Center, Connecticut, Farmington 06030, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shultz</LastName><ForeName>L D</ForeName><Initials>LD</Initials></Author><Author ValidYN="Y"><LastName>Rajan</LastName><ForeName>T V</ForeName><Initials>TV</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="N"><Grant><GrantID>AI30389</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI39705</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI42362</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Exp Parasitol</MedlineTA><NlmUniqueID>0370713</NlmUniqueID><ISSNLinking>0014-4894</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016693">Receptors, Antigen, T-Cell, alpha-beta</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017178" MajorTopicYN="N">Brugia malayi</DescriptorName><QualifierName UI="Q000254" MajorTopicYN="Y">growth & development</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004605" MajorTopicYN="N">Elephantiasis, Filarial</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000469" MajorTopicYN="N">parasitology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006790" MajorTopicYN="N">Host-Parasite Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007121" MajorTopicYN="N">Immunocompetence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016867" MajorTopicYN="N">Immunocompromised Host</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016513" MajorTopicYN="N">Mice, SCID</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016693" MajorTopicYN="N">Receptors, Antigen, T-Cell, alpha-beta</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013601" MajorTopicYN="N">T-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1999</Year><Month>8</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1999</Year><Month>8</Month><Day>28</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1999</Year><Month>8</Month><Day>28</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10464039</ArticleId><ArticleId IdType="doi">10.1006/expr.1999.4438</ArticleId><ArticleId IdType="pii">S0014-4894(99)94438-7</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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