DGK α and ζ Activities Control TH1 and TH17 Cell Differentiation.
Identifieur interne : 000367 ( Main/Exploration ); précédent : 000366; suivant : 000368DGK α and ζ Activities Control TH1 and TH17 Cell Differentiation.
Auteurs : Jialong Yang [États-Unis] ; Hong-Xia Wang [États-Unis] ; Jinhai Xie [États-Unis] ; Lei Li [États-Unis] ; Jinli Wang [États-Unis] ; Edwin C K. Wan [États-Unis] ; Xiao-Ping Zhong [États-Unis]Source :
- Frontiers in immunology [ 1664-3224 ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Cellules Th17 (cytologie), Cellules Th17 (immunologie), Complexe-1 cible mécanistique de la rapamycine (génétique), Complexe-1 cible mécanistique de la rapamycine (immunologie), Diacylglycérol kinase (génétique), Diacylglycérol kinase (immunologie), Différenciation cellulaire (génétique), Différenciation cellulaire (immunologie), Lymphocytes auxiliaires Th1 (cytologie), Lymphocytes auxiliaires Th1 (immunologie), Ribosomal Protein S6 Kinases, 90-kDa (génétique), Ribosomal Protein S6 Kinases, 90-kDa (immunologie), Souris (MeSH), Souris knockout (MeSH), Transduction du signal (génétique), Transduction du signal (immunologie).
- MESH :
- cytologie : Cellules Th17, Lymphocytes auxiliaires Th1.
- génétique : Complexe-1 cible mécanistique de la rapamycine, Diacylglycérol kinase, Différenciation cellulaire, Ribosomal Protein S6 Kinases, 90-kDa, Transduction du signal.
- immunologie : Cellules Th17, Complexe-1 cible mécanistique de la rapamycine, Diacylglycérol kinase, Différenciation cellulaire, Lymphocytes auxiliaires Th1, Ribosomal Protein S6 Kinases, 90-kDa, Transduction du signal.
- Animaux, Souris, Souris knockout.
English descriptors
- KwdEn :
- Animals (MeSH), Cell Differentiation (genetics), Cell Differentiation (immunology), Diacylglycerol Kinase (genetics), Diacylglycerol Kinase (immunology), Mechanistic Target of Rapamycin Complex 1 (genetics), Mechanistic Target of Rapamycin Complex 1 (immunology), Mice (MeSH), Mice, Knockout (MeSH), Ribosomal Protein S6 Kinases, 90-kDa (genetics), Ribosomal Protein S6 Kinases, 90-kDa (immunology), Signal Transduction (genetics), Signal Transduction (immunology), Th1 Cells (cytology), Th1 Cells (immunology), Th17 Cells (cytology), Th17 Cells (immunology).
- MESH :
- chemical , genetics : Diacylglycerol Kinase, Mechanistic Target of Rapamycin Complex 1, Ribosomal Protein S6 Kinases, 90-kDa.
- cytology : Th1 Cells, Th17 Cells.
- genetics : Cell Differentiation, Signal Transduction.
- immunology : Cell Differentiation, Diacylglycerol Kinase, Mechanistic Target of Rapamycin Complex 1, Ribosomal Protein S6 Kinases, 90-kDa, Signal Transduction, Th1 Cells, Th17 Cells.
- Animals, Mice, Mice, Knockout.
Abstract
CD4+ T helper (TH) cells are critical for protective adaptive immunity against pathogens, and they also contribute to the pathogenesis of autoimmune diseases. How TH differentiation is regulated by the TCR's downstream signaling is still poorly understood. We describe here that diacylglycerol kinases (DGKs), which are enzymes that convert diacylglycerol (DAG) to phosphatidic acid, exert differential effects on TH cell differentiation in a DGK dosage-dependent manner. A deficiency of either DGKα or ζ selectively impaired TH1 differentiation without obviously affecting TH2 and TH17 differentiation. However, simultaneous ablation of both DGKα and ζ promoted TH1 and TH17 differentiation in vitro and in vivo, leading to exacerbated airway inflammation. Furthermore, we demonstrate that dysregulation of TH17 differentiation of DGKα and ζ double-deficient CD4+ T cells was, at least in part, caused by increased mTOR complex 1/S6K1 signaling.
DOI: 10.3389/fimmu.2019.03048
PubMed: 32010133
PubMed Central: PMC6974463
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC</wicri:regionArea><placeName><region type="state">Caroline du Nord</region></placeName></affiliation></author><author><name sortKey="Wang, Hong Xia" sort="Wang, Hong Xia" uniqKey="Wang H" first="Hong-Xia" last="Wang">Hong-Xia Wang</name><affiliation wicri:level="2"><nlm:affiliation>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC</wicri:regionArea><placeName><region type="state">Caroline du Nord</region></placeName></affiliation></author><author><name sortKey="Xie, Jinhai" sort="Xie, Jinhai" uniqKey="Xie J" first="Jinhai" last="Xie">Jinhai Xie</name><affiliation wicri:level="2"><nlm:affiliation>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC</wicri:regionArea><placeName><region type="state">Caroline du Nord</region></placeName></affiliation></author><author><name sortKey="Li, Lei" sort="Li, Lei" uniqKey="Li L" first="Lei" last="Li">Lei Li</name><affiliation wicri:level="2"><nlm:affiliation>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC</wicri:regionArea><placeName><region type="state">Caroline du Nord</region></placeName></affiliation></author><author><name sortKey="Wang, Jinli" sort="Wang, Jinli" uniqKey="Wang J" first="Jinli" last="Wang">Jinli Wang</name><affiliation wicri:level="2"><nlm:affiliation>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC</wicri:regionArea><placeName><region type="state">Caroline du Nord</region></placeName></affiliation></author><author><name sortKey="Wan, Edwin C K" sort="Wan, Edwin C K" uniqKey="Wan E" first="Edwin C K" last="Wan">Edwin C K. Wan</name><affiliation wicri:level="2"><nlm:affiliation>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC</wicri:regionArea><placeName><region type="state">Caroline du Nord</region></placeName></affiliation><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology, Immunology, and Cell Biology, West Virginia University School of Medicine, Morgantown, WV, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology, Immunology, and Cell Biology, West Virginia University School of Medicine, Morgantown, WV</wicri:regionArea><placeName><region type="state">Virginie-Occidentale</region></placeName></affiliation><affiliation wicri:level="2"><nlm:affiliation>Department of Neuroscience, West Virginia University School of Medicine, Morgantown, WV, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neuroscience, West Virginia University School of Medicine, Morgantown, WV</wicri:regionArea><placeName><region type="state">Virginie-Occidentale</region></placeName></affiliation></author><author><name sortKey="Zhong, Xiao Ping" sort="Zhong, Xiao Ping" uniqKey="Zhong X" first="Xiao-Ping" last="Zhong">Xiao-Ping Zhong</name><affiliation wicri:level="2"><nlm:affiliation>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC</wicri:regionArea><placeName><region type="state">Caroline du Nord</region></placeName></affiliation><affiliation wicri:level="2"><nlm:affiliation>Department of Immunology, Duke University Medical Center, Durham, NC, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Immunology, Duke University Medical Center, Durham, NC</wicri:regionArea><placeName><region type="state">Caroline du Nord</region></placeName></affiliation><affiliation wicri:level="2"><nlm:affiliation>Hematologic Malignancies and Cellular Therapies Program, Duke Cancer Institute, Duke University Medical Center, Durham, NC, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Hematologic Malignancies and Cellular Therapies Program, Duke Cancer Institute, Duke University Medical Center, Durham, NC</wicri:regionArea><placeName><region type="state">Caroline du Nord</region></placeName></affiliation></author></analytic><series><title level="j">Frontiers in immunology</title><idno type="eISSN">1664-3224</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Cell Differentiation (genetics)</term><term>Cell Differentiation (immunology)</term><term>Diacylglycerol Kinase (genetics)</term><term>Diacylglycerol Kinase (immunology)</term><term>Mechanistic Target of Rapamycin Complex 1 (genetics)</term><term>Mechanistic Target of Rapamycin Complex 1 (immunology)</term><term>Mice (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Ribosomal Protein S6 Kinases, 90-kDa (genetics)</term><term>Ribosomal Protein S6 Kinases, 90-kDa (immunology)</term><term>Signal Transduction (genetics)</term><term>Signal Transduction (immunology)</term><term>Th1 Cells (cytology)</term><term>Th1 Cells (immunology)</term><term>Th17 Cells (cytology)</term><term>Th17 Cells (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Cellules Th17 (cytologie)</term><term>Cellules Th17 (immunologie)</term><term>Complexe-1 cible mécanistique de la rapamycine (génétique)</term><term>Complexe-1 cible mécanistique de la rapamycine (immunologie)</term><term>Diacylglycérol kinase (génétique)</term><term>Diacylglycérol kinase (immunologie)</term><term>Différenciation cellulaire (génétique)</term><term>Différenciation cellulaire (immunologie)</term><term>Lymphocytes auxiliaires Th1 (cytologie)</term><term>Lymphocytes auxiliaires Th1 (immunologie)</term><term>Ribosomal Protein S6 Kinases, 90-kDa (génétique)</term><term>Ribosomal Protein S6 Kinases, 90-kDa (immunologie)</term><term>Souris (MeSH)</term><term>Souris knockout (MeSH)</term><term>Transduction du signal (génétique)</term><term>Transduction du signal (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Diacylglycerol Kinase</term><term>Mechanistic Target of Rapamycin Complex 1</term><term>Ribosomal Protein S6 Kinases, 90-kDa</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules Th17</term><term>Lymphocytes auxiliaires Th1</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Th1 Cells</term><term>Th17 Cells</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Differentiation</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Complexe-1 cible mécanistique de la rapamycine</term><term>Diacylglycérol kinase</term><term>Différenciation cellulaire</term><term>Ribosomal Protein S6 Kinases, 90-kDa</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules Th17</term><term>Complexe-1 cible mécanistique de la rapamycine</term><term>Diacylglycérol kinase</term><term>Différenciation cellulaire</term><term>Lymphocytes auxiliaires Th1</term><term>Ribosomal Protein S6 Kinases, 90-kDa</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Cell Differentiation</term><term>Diacylglycerol Kinase</term><term>Mechanistic Target of Rapamycin Complex 1</term><term>Ribosomal Protein S6 Kinases, 90-kDa</term><term>Signal Transduction</term><term>Th1 Cells</term><term>Th17 Cells</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Mice</term><term>Mice, Knockout</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Souris</term><term>Souris knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">CD4<sup>+</sup> T helper (T<sub>H</sub>) cells are critical for protective adaptive immunity against pathogens, and they also contribute to the pathogenesis of autoimmune diseases. How T<sub>H</sub> differentiation is regulated by the TCR's downstream signaling is still poorly understood. We describe here that diacylglycerol kinases (DGKs), which are enzymes that convert diacylglycerol (DAG) to phosphatidic acid, exert differential effects on T<sub>H</sub> cell differentiation in a DGK dosage-dependent manner. A deficiency of either DGKα or ζ selectively impaired T<sub>H</sub>1 differentiation without obviously affecting T<sub>H</sub>2 and T<sub>H</sub>17 differentiation. However, simultaneous ablation of both DGKα and ζ promoted T<sub>H</sub>1 and T<sub>H</sub>17 differentiation <i>in vitro</i> and <i>in vivo</i>, leading to exacerbated airway inflammation. Furthermore, we demonstrate that dysregulation of T<sub>H</sub>17 differentiation of DGKα and ζ double-deficient CD4<sup>+</sup> T cells was, at least in part, caused by increased mTOR complex 1/S6K1 signaling.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32010133</PMID><DateCompleted><Year>2020</Year><Month>10</Month><Day>22</Day></DateCompleted><DateRevised><Year>2020</Year><Month>10</Month><Day>22</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1664-3224</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><PubDate><Year>2019</Year></PubDate></JournalIssue><Title>Frontiers in immunology</Title><ISOAbbreviation>Front Immunol</ISOAbbreviation></Journal><ArticleTitle>DGK α and ζ Activities Control T<sub>H</sub>1 and T<sub>H</sub>17 Cell Differentiation.</ArticleTitle><Pagination><MedlinePgn>3048</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3389/fimmu.2019.03048</ELocationID><Abstract><AbstractText>CD4<sup>+</sup> T helper (T<sub>H</sub>) cells are critical for protective adaptive immunity against pathogens, and they also contribute to the pathogenesis of autoimmune diseases. How T<sub>H</sub> differentiation is regulated by the TCR's downstream signaling is still poorly understood. We describe here that diacylglycerol kinases (DGKs), which are enzymes that convert diacylglycerol (DAG) to phosphatidic acid, exert differential effects on T<sub>H</sub> cell differentiation in a DGK dosage-dependent manner. A deficiency of either DGKα or ζ selectively impaired T<sub>H</sub>1 differentiation without obviously affecting T<sub>H</sub>2 and T<sub>H</sub>17 differentiation. However, simultaneous ablation of both DGKα and ζ promoted T<sub>H</sub>1 and T<sub>H</sub>17 differentiation <i>in vitro</i> and <i>in vivo</i>, leading to exacerbated airway inflammation. Furthermore, we demonstrate that dysregulation of T<sub>H</sub>17 differentiation of DGKα and ζ double-deficient CD4<sup>+</sup> T cells was, at least in part, caused by increased mTOR complex 1/S6K1 signaling.</AbstractText><CopyrightInformation>Copyright © 2020 Yang, Wang, Xie, Li, Wang, Wan and Zhong.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Jialong</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Hong-Xia</ForeName><Initials>HX</Initials><AffiliationInfo><Affiliation>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xie</LastName><ForeName>Jinhai</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Lei</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Jinli</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wan</LastName><ForeName>Edwin C K</ForeName><Initials>ECK</Initials><AffiliationInfo><Affiliation>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Microbiology, Immunology, and Cell Biology, West Virginia University School of Medicine, Morgantown, WV, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Neuroscience, West Virginia University School of Medicine, Morgantown, WV, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhong</LastName><ForeName>Xiao-Ping</ForeName><Initials>XP</Initials><AffiliationInfo><Affiliation>Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Immunology, Duke University Medical Center, Durham, NC, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hematologic Malignancies and Cellular Therapies Program, Duke Cancer Institute, Duke University Medical Center, Durham, NC, United States.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 AI079088</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI101206</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R56 AG060984</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>01</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front 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