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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<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>
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<author><name sortKey="Shultz, L D" sort="Shultz, L D" uniqKey="Shultz L" first="L D" last="Shultz">L D Shultz</name>
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<author><name sortKey="Rajan, T V" sort="Rajan, T V" uniqKey="Rajan T" first="T V" last="Rajan">T V Rajan</name>
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<affiliation><nlm:affiliation>Department of Pathology, University of Connecticut Health Center, Connecticut, Farmington 06030, USA.</nlm:affiliation>
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<author><name sortKey="Shultz, L D" sort="Shultz, L D" uniqKey="Shultz L" first="L D" last="Shultz">L D Shultz</name>
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<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>
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<keywords scheme="MESH" qualifier="parasitology" xml:lang="en"><term>Elephantiasis, Filarial</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>T-Lymphocytes</term>
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<term>Host-Parasite Interactions</term>
<term>Immunocompetence</term>
<term>Immunocompromised Host</term>
<term>Mice</term>
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<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>
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<Title>Experimental parasitology</Title>
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<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>
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