RapamycinFungusV1, Main, Exploration, bibRecord, 000410

4-1BB Regulates Effector CD8 T Cell Accumulation in the Lung Tissue through a TRAF1-, mTOR-, and Antigen-Dependent Mechanism to Enhance Tissue-Resident Memory T Cell Formation during Respiratory Influenza Infection.

Identifieur interne : 000410 ( Main/Exploration ); précédent : 000409; suivant : 000411

4-1BB Regulates Effector CD8 T Cell Accumulation in the Lung Tissue through a TRAF1-, mTOR-, and Antigen-Dependent Mechanism to Enhance Tissue-Resident Memory T Cell Formation during Respiratory Influenza Infection.

Auteurs : Angela C. Zhou [Canada] ; Nathália V. Batista [Canada] ; Tania H. Watts [Canada]

Source :

Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2019.

RBID : pubmed:30867239

Descripteurs français

English descriptors

KwdEn :
- 4-1BB Ligand (genetics), 4-1BB Ligand (immunology), Animals (MeSH), CD8-Positive T-Lymphocytes (immunology), CD8-Positive T-Lymphocytes (pathology), Immunologic Memory (MeSH), Influenza A virus (immunology), Lung (immunology), Lung (pathology), Lung (virology), Lung Diseases (genetics), Lung Diseases (immunology), Lung Diseases (pathology), Lung Diseases (virology), Mice (MeSH), Mice, Knockout (MeSH), Orthomyxoviridae Infections (genetics), Orthomyxoviridae Infections (immunology), Orthomyxoviridae Infections (pathology), TNF Receptor-Associated Factor 1 (genetics), TNF Receptor-Associated Factor 1 (immunology), TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (immunology).
MESH :
- chemical , genetics : 4-1BB Ligand, TNF Receptor-Associated Factor 1, TOR Serine-Threonine Kinases.
- chemical , immunology : 4-1BB Ligand, TNF Receptor-Associated Factor 1, TOR Serine-Threonine Kinases.
- genetics : Lung Diseases, Orthomyxoviridae Infections.
- immunology : CD8-Positive T-Lymphocytes, Influenza A virus, Lung, Lung Diseases, Orthomyxoviridae Infections.
- pathology : CD8-Positive T-Lymphocytes, Lung, Lung Diseases, Orthomyxoviridae Infections.
- virology : Lung, Lung Diseases.
- Animals, Immunologic Memory, Mice, Mice, Knockout.

Abstract

The TNFR superfamily member 4-1BB is important in the establishment of tissue-resident memory T cells (Trm) in the lung tissue following influenza infection. Moreover, supraphysiological boosting of 4-1BB in the airways during the boost phase of a prime-boost immunization regimen increases the long-lived Trm population, correlating with increased protection against heterotypic challenge. However, little is known about how 4-1BB contributes to the establishment of the lung Trm population. In this study, we show that effects of 4-1BB on lung Trm accumulation are already apparent at the effector stage, suggesting that the major role of 4-1BB in Trm formation is to allow persistence of CD8 T effector cells in the lung as they transition to Trm. Using supraphysiological stimulation of 4-1BB in the boost phase of a prime-boost immunization, we show that the effect of 4-1BB on Trm generation requires local delivery of both Ag and costimulation, is inhibited by rapamycin treatment during secondary CD8 effector T cell expansion, and is dependent on the signaling adaptor TRAF1. The decrease in lung Trm following early rapamycin treatment is accompanied by increased circulating memory T cells, as well as fewer effectors, suggesting a role for mammalian target of rapamycin (mTOR) in the formation of Trm through effects on the accumulation of effector precursors. Taken together, these data point to an important role for 4-1BB, TRAF1, and mTOR in the persistence of CD8 effector T cells in the lung parenchyma, thereby allowing the transition to Trm.

DOI: 10.4049/jimmunol.1800795
PubMed: 30867239

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000321
to stream Main, to step Curation: 000321

Le document en format XML

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<term>CD8-Positive T-Lymphocytes (immunology)</term>
<term>CD8-Positive T-Lymphocytes (pathology)</term>
<term>Immunologic Memory (MeSH)</term>
<term>Influenza A virus (immunology)</term>
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<term>Lung (pathology)</term>
<term>Lung (virology)</term>
<term>Lung Diseases (genetics)</term>
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<term>Lung Diseases (pathology)</term>
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<term>Mice (MeSH)</term>
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<term>Orthomyxoviridae Infections (pathology)</term>
<term>TNF Receptor-Associated Factor 1 (genetics)</term>
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<term>TOR Serine-Threonine Kinases (immunology)</term>
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<term>Facteur-1 associé aux récepteurs de TNF (immunologie)</term>
<term>Infections à Orthomyxoviridae (anatomopathologie)</term>
<term>Infections à Orthomyxoviridae (génétique)</term>
<term>Infections à Orthomyxoviridae (immunologie)</term>
<term>Ligand de 4-1BB (génétique)</term>
<term>Ligand de 4-1BB (immunologie)</term>
<term>Lymphocytes T CD8+ (anatomopathologie)</term>
<term>Lymphocytes T CD8+ (immunologie)</term>
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<term>Maladies pulmonaires (génétique)</term>
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<front><div type="abstract" xml:lang="en">The TNFR superfamily member 4-1BB is important in the establishment of tissue-resident memory T cells (Trm) in the lung tissue following influenza infection. Moreover, supraphysiological boosting of 4-1BB in the airways during the boost phase of a prime-boost immunization regimen increases the long-lived Trm population, correlating with increased protection against heterotypic challenge. However, little is known about how 4-1BB contributes to the establishment of the lung Trm population. In this study, we show that effects of 4-1BB on lung Trm accumulation are already apparent at the effector stage, suggesting that the major role of 4-1BB in Trm formation is to allow persistence of CD8 T effector cells in the lung as they transition to Trm. Using supraphysiological stimulation of 4-1BB in the boost phase of a prime-boost immunization, we show that the effect of 4-1BB on Trm generation requires local delivery of both Ag and costimulation, is inhibited by rapamycin treatment during secondary CD8 effector T cell expansion, and is dependent on the signaling adaptor TRAF1. The decrease in lung Trm following early rapamycin treatment is accompanied by increased circulating memory T cells, as well as fewer effectors, suggesting a role for mammalian target of rapamycin (mTOR) in the formation of Trm through effects on the accumulation of effector precursors. Taken together, these data point to an important role for 4-1BB, TRAF1, and mTOR in the persistence of CD8 effector T cells in the lung parenchyma, thereby allowing the transition to Trm.</div>
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<Abstract><AbstractText>The TNFR superfamily member 4-1BB is important in the establishment of tissue-resident memory T cells (Trm) in the lung tissue following influenza infection. Moreover, supraphysiological boosting of 4-1BB in the airways during the boost phase of a prime-boost immunization regimen increases the long-lived Trm population, correlating with increased protection against heterotypic challenge. However, little is known about how 4-1BB contributes to the establishment of the lung Trm population. In this study, we show that effects of 4-1BB on lung Trm accumulation are already apparent at the effector stage, suggesting that the major role of 4-1BB in Trm formation is to allow persistence of CD8 T effector cells in the lung as they transition to Trm. Using supraphysiological stimulation of 4-1BB in the boost phase of a prime-boost immunization, we show that the effect of 4-1BB on Trm generation requires local delivery of both Ag and costimulation, is inhibited by rapamycin treatment during secondary CD8 effector T cell expansion, and is dependent on the signaling adaptor TRAF1. The decrease in lung Trm following early rapamycin treatment is accompanied by increased circulating memory T cells, as well as fewer effectors, suggesting a role for mammalian target of rapamycin (mTOR) in the formation of Trm through effects on the accumulation of effector precursors. Taken together, these data point to an important role for 4-1BB, TRAF1, and mTOR in the persistence of CD8 effector T cells in the lung parenchyma, thereby allowing the transition to Trm.</AbstractText>
<CopyrightInformation>Copyright © 2019 by The American Association of Immunologists, Inc.</CopyrightInformation>
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<name sortKey="Batista, Nathalia V" sort="Batista, Nathalia V" uniqKey="Batista N" first="Nathália V" last="Batista">Nathália V. Batista</name>
<name sortKey="Watts, Tania H" sort="Watts, Tania H" uniqKey="Watts T" first="Tania H" last="Watts">Tania H. Watts</name>
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EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000410 | SxmlIndent | more

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{{Explor lien
   |wiki=    Bois
   |area=    RapamycinFungusV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:30867239
   |texte=   4-1BB Regulates Effector CD8 T Cell Accumulation in the Lung Tissue through a TRAF1-, mTOR-, and Antigen-Dependent Mechanism to Enhance Tissue-Resident Memory T Cell Formation during Respiratory Influenza Infection.
}}

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HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i   -Sk "pubmed:30867239" \
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       | NlmPubMed2Wicri -a RapamycinFungusV1

This area was generated with Dilib version V0.6.38.
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	Serveur d'exploration sur la rapamycine et les champignons
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur la rapamycine et les champignons

4-1BB Regulates Effector CD8 T Cell Accumulation in the Lung Tissue through a TRAF1-, mTOR-, and Antigen-Dependent Mechanism to Enhance Tissue-Resident Memory T Cell Formation during Respiratory Influenza Infection.

4-1BB Regulates Effector CD8 T Cell Accumulation in the Lung Tissue through a TRAF1-, mTOR-, and Antigen-Dependent Mechanism to Enhance Tissue-Resident Memory T Cell Formation during Respiratory Influenza Infection.

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