Chronic heat stress inhibits immune responses to H5N1 vaccination through regulating CD4⁺ CD25⁺ Foxp3⁺ Tregs.
Identifieur interne : 000606 ( Ncbi/Checkpoint ); précédent : 000605; suivant : 000607Chronic heat stress inhibits immune responses to H5N1 vaccination through regulating CD4⁺ CD25⁺ Foxp3⁺ Tregs.
Auteurs : Di Meng [République populaire de Chine] ; Yanxin Hu ; Chong Xiao ; Tangting Wei ; Qiang Zou ; Ming WangSource :
- BioMed research international [ 2314-6141 ] ; 2013.
Descripteurs français
- KwdFr :
- Facteur de croissance transformant bêta (immunologie), Facteur de croissance transformant bêta (métabolisme), Facteurs de transcription Forkhead (immunologie), Facteurs de transcription Forkhead (métabolisme), Grippe humaine (anatomopathologie), Grippe humaine (métabolisme), Grippe humaine (virologie), Humains, Immunosuppression thérapeutique, Lymphocytes T CD4+ (immunologie), Lymphocytes T CD4+ (métabolisme), Lymphocytes T régulateurs (immunologie), Lymphocytes T régulateurs (métabolisme), Réaction de choc thermique (immunologie), Sous-type H5N1 du virus de la grippe A (immunologie), Sous-type H5N1 du virus de la grippe A (pathogénicité), Sous-unité alpha du récepteur à l'interleukine-2 (immunologie), Sous-unité alpha du récepteur à l'interleukine-2 (métabolisme), Température élevée, Vaccination.
- MESH :
- anatomopathologie : Grippe humaine.
- immunologie : Facteur de croissance transformant bêta, Facteurs de transcription Forkhead, Lymphocytes T CD4+, Lymphocytes T régulateurs, Réaction de choc thermique, Sous-type H5N1 du virus de la grippe A, Sous-unité alpha du récepteur à l'interleukine-2.
- métabolisme : Facteur de croissance transformant bêta, Facteurs de transcription Forkhead, Grippe humaine, Lymphocytes T CD4+, Lymphocytes T régulateurs, Sous-unité alpha du récepteur à l'interleukine-2.
- pathogénicité : Sous-type H5N1 du virus de la grippe A.
- virologie : Grippe humaine.
- Humains, Immunosuppression thérapeutique, Température élevée, Vaccination.
English descriptors
- KwdEn :
- CD4-Positive T-Lymphocytes (immunology), CD4-Positive T-Lymphocytes (metabolism), Forkhead Transcription Factors (immunology), Forkhead Transcription Factors (metabolism), Heat-Shock Response (immunology), Hot Temperature, Humans, Immunosuppression, Influenza A Virus, H5N1 Subtype (immunology), Influenza A Virus, H5N1 Subtype (pathogenicity), Influenza, Human (metabolism), Influenza, Human (pathology), Influenza, Human (virology), Interleukin-2 Receptor alpha Subunit (immunology), Interleukin-2 Receptor alpha Subunit (metabolism), T-Lymphocytes, Regulatory (immunology), T-Lymphocytes, Regulatory (metabolism), Transforming Growth Factor beta (immunology), Transforming Growth Factor beta (metabolism), Vaccination.
- MESH :
- chemical , immunology : Forkhead Transcription Factors, Interleukin-2 Receptor alpha Subunit, Transforming Growth Factor beta.
- immunology : CD4-Positive T-Lymphocytes, Heat-Shock Response, Influenza A Virus, H5N1 Subtype, T-Lymphocytes, Regulatory.
- metabolism : CD4-Positive T-Lymphocytes, Forkhead Transcription Factors, Influenza, Human, Interleukin-2 Receptor alpha Subunit, T-Lymphocytes, Regulatory, Transforming Growth Factor beta.
- pathogenicity : Influenza A Virus, H5N1 Subtype.
- pathology : Influenza, Human.
- virology : Influenza, Human.
- Hot Temperature, Humans, Immunosuppression, Vaccination.
Abstract
Chronic heat stress (CHS) is known to have negative impacts on the immune responses in animals and increases their susceptibility to infections including the highly pathogenic avian influenza virus H5N1. However, the role of regulatory T cells (Tregs) in CHS immunosuppression remains largely undefined. In this study, we demonstrated a novel mechanism by which CHS suppressed both Th1 and Th2 immune responses and dramatically decreased the protective efficacy of the formalin-inactivated H5N1 vaccine against H5N1 influenza virus infection. This suppression was found to be associated with the induced generation of CD4⁺ CD25⁺ Foxp3⁺ Tregs and the increased secretions of IL-10 and TGF- β in CD4⁺ T cells. Adoptive transfer of the induced Tregs also suppressed the protective efficacy of formalin-inactivated H5N1 virus immunization. Collectively, this study identifies a novel mechanism of CHS immunosuppression mediated by regulating CD4⁺ CD25⁺ Foxp3⁺ Tregs.
DOI: 10.1155/2013/160859
PubMed: 24151582
Affiliations:
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pubmed:24151582Le document en format XML
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de la grippe A</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Influenza, Human</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Grippe humaine</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Influenza, Human</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Hot Temperature</term><term>Humans</term><term>Immunosuppression</term><term>Vaccination</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Humains</term><term>Immunosuppression thérapeutique</term><term>Température élevée</term><term>Vaccination</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Chronic heat stress (CHS) is known to have negative impacts on the immune responses in animals and increases their susceptibility to infections including the highly pathogenic avian influenza virus H5N1. However, the role of regulatory T cells (Tregs) in CHS immunosuppression remains largely undefined. In this study, we demonstrated a novel mechanism by which CHS suppressed both Th1 and Th2 immune responses and dramatically decreased the protective efficacy of the formalin-inactivated H5N1 vaccine against H5N1 influenza virus infection. This suppression was found to be associated with the induced generation of CD4⁺ CD25⁺ Foxp3⁺ Tregs and the increased secretions of IL-10 and TGF- β in CD4⁺ T cells. Adoptive transfer of the induced Tregs also suppressed the protective efficacy of formalin-inactivated H5N1 virus immunization. Collectively, this study identifies a novel mechanism of CHS immunosuppression mediated by regulating CD4⁺ CD25⁺ Foxp3⁺ Tregs.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country><settlement><li>Pékin</li></settlement></list><tree><noCountry><name sortKey="Hu, Yanxin" sort="Hu, Yanxin" uniqKey="Hu Y" first="Yanxin" last="Hu">Yanxin Hu</name><name sortKey="Wang, Ming" sort="Wang, Ming" uniqKey="Wang M" first="Ming" last="Wang">Ming Wang</name><name sortKey="Wei, Tangting" sort="Wei, Tangting" uniqKey="Wei T" first="Tangting" last="Wei">Tangting Wei</name><name sortKey="Xiao, Chong" sort="Xiao, Chong" uniqKey="Xiao C" first="Chong" last="Xiao">Chong Xiao</name><name sortKey="Zou, Qiang" sort="Zou, Qiang" uniqKey="Zou Q" first="Qiang" last="Zou">Qiang Zou</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Meng, Di" sort="Meng, Di" uniqKey="Meng D" first="Di" last="Meng">Di Meng</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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