Reprogramming of Th1 cells into regulatory T cells through rewiring of the metabolic status.
Identifieur interne : 000504 ( Main/Exploration ); précédent : 000503; suivant : 000505Reprogramming of Th1 cells into regulatory T cells through rewiring of the metabolic status.
Auteurs : Mitsuhiro Kanamori [Japon] ; Hiroko Nakatsukasa [Japon] ; Minako Ito [Japon] ; Shunsuke Chikuma [Japon] ; Akihiko Yoshimura [Japon]Source :
- International immunology [ 1460-2377 ] ; 2018.
Descripteurs français
- KwdFr :
- Adulte (MeSH), Animaux (MeSH), Humains (MeSH), Lymphocytes T régulateurs (cytologie), Lymphocytes T régulateurs (immunologie), Lymphocytes T régulateurs (métabolisme), Lymphocytes auxiliaires Th1 (cytologie), Lymphocytes auxiliaires Th1 (immunologie), Lymphocytes auxiliaires Th1 (métabolisme), Mâle (MeSH), Reprogrammation cellulaire (MeSH), Souris (MeSH), Souris de lignée BALB C (MeSH), Souris de lignée C57BL (MeSH).
- MESH :
- cytologie : Lymphocytes T régulateurs, Lymphocytes auxiliaires Th1.
- immunologie : Lymphocytes T régulateurs, Lymphocytes auxiliaires Th1.
- métabolisme : Lymphocytes T régulateurs, Lymphocytes auxiliaires Th1.
- Adulte, Animaux, Humains, Mâle, Reprogrammation cellulaire, Souris, Souris de lignée BALB C, Souris de lignée C57BL.
English descriptors
- KwdEn :
- Adult (MeSH), Animals (MeSH), Cellular Reprogramming (MeSH), Humans (MeSH), Male (MeSH), Mice (MeSH), Mice, Inbred BALB C (MeSH), Mice, Inbred C57BL (MeSH), T-Lymphocytes, Regulatory (cytology), T-Lymphocytes, Regulatory (immunology), T-Lymphocytes, Regulatory (metabolism), Th1 Cells (cytology), Th1 Cells (immunology), Th1 Cells (metabolism).
- MESH :
- cytology : T-Lymphocytes, Regulatory, Th1 Cells.
- immunology : T-Lymphocytes, Regulatory, Th1 Cells.
- metabolism : T-Lymphocytes, Regulatory, Th1 Cells.
- Adult, Animals, Cellular Reprogramming, Humans, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL.
Abstract
T helper type 1 (Th1) cells form one of the most stable CD4 T-cell subsets, and direct conversion of fully differentiated Th1 to regulatory T (Treg) cells has been poorly investigated. Here, we established a culture method for inducing Foxp3 from Th1 cells of mice and humans. This is achieved simply by resting Th1 cells without T-cell receptor ligation before stimulation in the presence of transforming growth factor-beta (TGF-β). We named the resulting Th1-derived Foxp3+ cells Th1reg cells. Mouse Th1reg cells showed an inducible Treg-like phenotype and suppressive ability both in vitro and in vivo. Th1reg cells could also be induced from in vivo-developed mouse Th1 cells. Unexpectedly, the resting process enabled Foxp3 expression not through epigenetic changes at the locus, but through metabolic change resulting from reduced mammalian target of rapamycin complex 1 (mTORC1) activity. mTORC1 suppressed TGF-β-induced phosphorylation of Smad2/3 in Th1 cells, which was restored in rested cells. Our study warrants future research aiming at development of immunotherapy with Th1reg cells.
DOI: 10.1093/intimm/dxy043
PubMed: 29982622
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Reprogramming of Th1 cells into regulatory T cells through rewiring of the metabolic status.</title><author><name sortKey="Kanamori, Mitsuhiro" sort="Kanamori, Mitsuhiro" uniqKey="Kanamori M" first="Mitsuhiro" last="Kanamori">Mitsuhiro Kanamori</name><affiliation wicri:level="3"><nlm:affiliation>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Nakatsukasa, Hiroko" sort="Nakatsukasa, Hiroko" uniqKey="Nakatsukasa H" first="Hiroko" last="Nakatsukasa">Hiroko Nakatsukasa</name><affiliation wicri:level="3"><nlm:affiliation>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Ito, Minako" sort="Ito, Minako" uniqKey="Ito M" first="Minako" last="Ito">Minako Ito</name><affiliation wicri:level="3"><nlm:affiliation>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Chikuma, Shunsuke" sort="Chikuma, Shunsuke" uniqKey="Chikuma S" first="Shunsuke" last="Chikuma">Shunsuke Chikuma</name><affiliation wicri:level="3"><nlm:affiliation>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Yoshimura, Akihiko" sort="Yoshimura, Akihiko" uniqKey="Yoshimura A" first="Akihiko" last="Yoshimura">Akihiko Yoshimura</name><affiliation wicri:level="3"><nlm:affiliation>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2018">2018</date><idno type="RBID">pubmed:29982622</idno><idno type="pmid">29982622</idno><idno type="doi">10.1093/intimm/dxy043</idno><idno type="wicri:Area/Main/Corpus">000506</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000506</idno><idno type="wicri:Area/Main/Curation">000506</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000506</idno><idno type="wicri:Area/Main/Exploration">000506</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Reprogramming of Th1 cells into regulatory T cells through rewiring of the metabolic status.</title><author><name sortKey="Kanamori, Mitsuhiro" sort="Kanamori, Mitsuhiro" uniqKey="Kanamori M" first="Mitsuhiro" last="Kanamori">Mitsuhiro Kanamori</name><affiliation wicri:level="3"><nlm:affiliation>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Nakatsukasa, Hiroko" sort="Nakatsukasa, Hiroko" uniqKey="Nakatsukasa H" first="Hiroko" last="Nakatsukasa">Hiroko Nakatsukasa</name><affiliation wicri:level="3"><nlm:affiliation>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Ito, Minako" sort="Ito, Minako" uniqKey="Ito M" first="Minako" last="Ito">Minako Ito</name><affiliation wicri:level="3"><nlm:affiliation>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Chikuma, Shunsuke" sort="Chikuma, Shunsuke" uniqKey="Chikuma S" first="Shunsuke" last="Chikuma">Shunsuke Chikuma</name><affiliation wicri:level="3"><nlm:affiliation>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Yoshimura, Akihiko" sort="Yoshimura, Akihiko" uniqKey="Yoshimura A" first="Akihiko" last="Yoshimura">Akihiko Yoshimura</name><affiliation wicri:level="3"><nlm:affiliation>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author></analytic><series><title level="j">International immunology</title><idno type="eISSN">1460-2377</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult (MeSH)</term><term>Animals (MeSH)</term><term>Cellular Reprogramming (MeSH)</term><term>Humans (MeSH)</term><term>Male (MeSH)</term><term>Mice (MeSH)</term><term>Mice, Inbred BALB C (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>T-Lymphocytes, Regulatory (cytology)</term><term>T-Lymphocytes, Regulatory (immunology)</term><term>T-Lymphocytes, Regulatory (metabolism)</term><term>Th1 Cells (cytology)</term><term>Th1 Cells (immunology)</term><term>Th1 Cells (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adulte (MeSH)</term><term>Animaux (MeSH)</term><term>Humains (MeSH)</term><term>Lymphocytes T régulateurs (cytologie)</term><term>Lymphocytes T régulateurs (immunologie)</term><term>Lymphocytes T régulateurs (métabolisme)</term><term>Lymphocytes auxiliaires Th1 (cytologie)</term><term>Lymphocytes auxiliaires Th1 (immunologie)</term><term>Lymphocytes auxiliaires Th1 (métabolisme)</term><term>Mâle (MeSH)</term><term>Reprogrammation cellulaire (MeSH)</term><term>Souris (MeSH)</term><term>Souris de lignée BALB C (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Lymphocytes T régulateurs</term><term>Lymphocytes auxiliaires Th1</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>T-Lymphocytes, Regulatory</term><term>Th1 Cells</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Lymphocytes T régulateurs</term><term>Lymphocytes auxiliaires Th1</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>T-Lymphocytes, Regulatory</term><term>Th1 Cells</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>T-Lymphocytes, Regulatory</term><term>Th1 Cells</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Lymphocytes T régulateurs</term><term>Lymphocytes auxiliaires Th1</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Animals</term><term>Cellular Reprogramming</term><term>Humans</term><term>Male</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Mice, Inbred C57BL</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Animaux</term><term>Humains</term><term>Mâle</term><term>Reprogrammation cellulaire</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Souris de lignée C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">T helper type 1 (Th1) cells form one of the most stable CD4 T-cell subsets, and direct conversion of fully differentiated Th1 to regulatory T (Treg) cells has been poorly investigated. Here, we established a culture method for inducing Foxp3 from Th1 cells of mice and humans. This is achieved simply by resting Th1 cells without T-cell receptor ligation before stimulation in the presence of transforming growth factor-beta (TGF-β). We named the resulting Th1-derived Foxp3+ cells Th1reg cells. Mouse Th1reg cells showed an inducible Treg-like phenotype and suppressive ability both in vitro and in vivo. Th1reg cells could also be induced from in vivo-developed mouse Th1 cells. Unexpectedly, the resting process enabled Foxp3 expression not through epigenetic changes at the locus, but through metabolic change resulting from reduced mammalian target of rapamycin complex 1 (mTORC1) activity. mTORC1 suppressed TGF-β-induced phosphorylation of Smad2/3 in Th1 cells, which was restored in rested cells. Our study warrants future research aiming at development of immunotherapy with Th1reg cells.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29982622</PMID><DateCompleted><Year>2019</Year><Month>08</Month><Day>05</Day></DateCompleted><DateRevised><Year>2019</Year><Month>08</Month><Day>05</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1460-2377</ISSN><JournalIssue CitedMedium="Internet"><Volume>30</Volume><Issue>8</Issue><PubDate><Year>2018</Year><Month>07</Month><Day>24</Day></PubDate></JournalIssue><Title>International immunology</Title><ISOAbbreviation>Int Immunol</ISOAbbreviation></Journal><ArticleTitle>Reprogramming of Th1 cells into regulatory T cells through rewiring of the metabolic status.</ArticleTitle><Pagination><MedlinePgn>357-373</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/intimm/dxy043</ELocationID><Abstract><AbstractText>T helper type 1 (Th1) cells form one of the most stable CD4 T-cell subsets, and direct conversion of fully differentiated Th1 to regulatory T (Treg) cells has been poorly investigated. Here, we established a culture method for inducing Foxp3 from Th1 cells of mice and humans. This is achieved simply by resting Th1 cells without T-cell receptor ligation before stimulation in the presence of transforming growth factor-beta (TGF-β). We named the resulting Th1-derived Foxp3+ cells Th1reg cells. Mouse Th1reg cells showed an inducible Treg-like phenotype and suppressive ability both in vitro and in vivo. Th1reg cells could also be induced from in vivo-developed mouse Th1 cells. Unexpectedly, the resting process enabled Foxp3 expression not through epigenetic changes at the locus, but through metabolic change resulting from reduced mammalian target of rapamycin complex 1 (mTORC1) activity. mTORC1 suppressed TGF-β-induced phosphorylation of Smad2/3 in Th1 cells, which was restored in rested cells. Our study warrants future research aiming at development of immunotherapy with Th1reg cells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kanamori</LastName><ForeName>Mitsuhiro</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nakatsukasa</LastName><ForeName>Hiroko</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ito</LastName><ForeName>Minako</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chikuma</LastName><ForeName>Shunsuke</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yoshimura</LastName><ForeName>Akihiko</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><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><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D065150" MajorTopicYN="Y">Cellular Reprogramming</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</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="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050378" MajorTopicYN="N">T-Lymphocytes, Regulatory</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="Y">cytology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018417" MajorTopicYN="N">Th1 Cells</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="Y">cytology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>05</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>06</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>7</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>8</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>7</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29982622</ArticleId><ArticleId IdType="pii">5047431</ArticleId><ArticleId IdType="doi">10.1093/intimm/dxy043</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Japon</li></country><region><li>Région de Kantō</li></region><settlement><li>Tokyo</li></settlement></list><tree><country name="Japon"><region name="Région de Kantō"><name sortKey="Kanamori, Mitsuhiro" sort="Kanamori, Mitsuhiro" uniqKey="Kanamori M" first="Mitsuhiro" last="Kanamori">Mitsuhiro Kanamori</name></region><name sortKey="Chikuma, Shunsuke" sort="Chikuma, Shunsuke" uniqKey="Chikuma S" first="Shunsuke" last="Chikuma">Shunsuke Chikuma</name><name sortKey="Ito, Minako" sort="Ito, Minako" uniqKey="Ito M" first="Minako" last="Ito">Minako Ito</name><name sortKey="Nakatsukasa, Hiroko" sort="Nakatsukasa, Hiroko" uniqKey="Nakatsukasa H" first="Hiroko" last="Nakatsukasa">Hiroko Nakatsukasa</name><name sortKey="Yoshimura, Akihiko" sort="Yoshimura, Akihiko" uniqKey="Yoshimura A" first="Akihiko" last="Yoshimura">Akihiko Yoshimura</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000504 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000504 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Bois
|area= RapamycinFungusV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:29982622
|texte= Reprogramming of Th1 cells into regulatory T cells through rewiring of the metabolic status.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:29982622" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a RapamycinFungusV1
| This area was generated with Dilib version V0.6.38. |  |