DGK α and ζ Activities Control TH1 and TH17 Cell Differentiation

CD4 + T helper (T H ) cells are critical for protective adaptive immunity against pathogens, and they also contribute to the pathogenesis of autoimmune diseases. How T H differentiation is regulated by the TCR's downstream signaling is still poorly understood. We describe here that diacylglycer...

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Published inFrontiers in immunology Vol. 10; p. 3048
Main Authors Yang, Jialong, Wang, Hong-Xia, Xie, Jinhai, Li, Lei, Wang, Jinli, Wan, Edwin C. K., Zhong, Xiao-Ping
Format Journal Article
LanguageEnglish
Published Frontiers Media S.A 15.01.2020
Subjects
airway inflammation
DGK
Immunology
mTOR
Th differentiation
Th1
Th17
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Abstract CD4 + T helper (T H ) cells are critical for protective adaptive immunity against pathogens, and they also contribute to the pathogenesis of autoimmune diseases. How T H 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 H cell differentiation in a DGK dosage-dependent manner. A deficiency of either DGKα or ζ selectively impaired T H 1 differentiation without obviously affecting T H 2 and T H 17 differentiation. However, simultaneous ablation of both DGKα and ζ promoted T H 1 and T H 17 differentiation in vitro and in vivo , leading to exacerbated airway inflammation. Furthermore, we demonstrate that dysregulation of T H 17 differentiation of DGKα and ζ double-deficient CD4 + T cells was, at least in part, caused by increased mTOR complex 1/S6K1 signaling.
AbstractList CD4 + T helper (T H ) cells are critical for protective adaptive immunity against pathogens, and they also contribute to the pathogenesis of autoimmune diseases. How T H 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 H cell differentiation in a DGK dosage-dependent manner. A deficiency of either DGKα or ζ selectively impaired T H 1 differentiation without obviously affecting T H 2 and T H 17 differentiation. However, simultaneous ablation of both DGKα and ζ promoted T H 1 and T H 17 differentiation in vitro and in vivo , leading to exacerbated airway inflammation. Furthermore, we demonstrate that dysregulation of T H 17 differentiation of DGKα and ζ double-deficient CD4 + T cells was, at least in part, caused by increased mTOR complex 1/S6K1 signaling.
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.
Author Xie, Jinhai
Zhong, Xiao-Ping
Yang, Jialong
Wang, Hong-Xia
Wan, Edwin C. K.
Wang, Jinli
Li, Lei
AuthorAffiliation 3 Department of Neuroscience, West Virginia University School of Medicine , Morgantown, WV , United States
2 Department of Microbiology, Immunology, and Cell Biology, West Virginia University School of Medicine , Morgantown, WV , United States
5 Hematologic Malignancies and Cellular Therapies Program, Duke Cancer Institute, Duke University Medical Center , Durham, NC , United States
1 Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center , Durham, NC , United States
4 Department of Immunology, Duke University Medical Center , Durham, NC , United States
AuthorAffiliation_xml – name: 2 Department of Microbiology, Immunology, and Cell Biology, West Virginia University School of Medicine , Morgantown, WV , United States
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– name: 3 Department of Neuroscience, West Virginia University School of Medicine , Morgantown, WV , United States
– name: 5 Hematologic Malignancies and Cellular Therapies Program, Duke Cancer Institute, Duke University Medical Center , Durham, NC , United States
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Edited by: Hongbo Chi, St. Jude Children's Research Hospital, United States
Reviewed by: Xuexian Yang, University of New Mexico, United States; Greg M. Delgoffe, University of Pittsburgh, United States
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Snippet CD4 + T helper (T H ) cells are critical for protective adaptive immunity against pathogens, and they also contribute to the pathogenesis of autoimmune...
CD4+ T helper (TH) cells are critical for protective adaptive immunity against pathogens, and they also contribute to the pathogenesis of autoimmune diseases....
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SubjectTerms airway inflammation
DGK
Immunology
mTOR
Th differentiation
Th1
Th17
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Title DGK α and ζ Activities Control TH1 and TH17 Cell Differentiation
URI https://search.proquest.com/docview/2350369168
https://pubmed.ncbi.nlm.nih.gov/PMC6974463
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Volume 10
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