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T Cell Exit from Quiescence and Differentiation into Th2 Cells Depend on Raptor-mTORC1-Mediated Metabolic Reprogramming

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TLDR
The authors' studies identify a Raptor-mTORC1-dependent pathway linking signal-dependent metabolic reprogramming to quiescence exit, and this in turn coordinates lymphocyte activation and fate decisions in adaptive immunity.
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This article is published in Immunity.The article was published on 2013-12-12 and is currently open access. It has received 307 citations till now. The article focuses on the topics: T cell & Priming (immunology).

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Citations
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Journal ArticleDOI

T cell metabolism drives immunity

TL;DR: The role of lymphocyte metabolism on immune cell development and function and the importance of “goodtenance” in immune cell function is discussed.
Journal ArticleDOI

Metabolic Regulation of Immune Responses

TL;DR: A general framework for understanding how metabolism fuels and regulates the maturation of immune responses is provided and a better understanding of the metabolic checkpoints that control these transitions might provide new insights for modulating immunity in infection, cancer, or inflammatory disorders.
Journal ArticleDOI

Type 2 immunity in tissue repair and fibrosis

TL;DR: The mechanisms by which type 2 immunity contributes to tissue regeneration and fibrosis following injury are discussed.
Journal ArticleDOI

Unraveling the Complex Interplay Between T Cell Metabolism and Function

TL;DR: How T cell metabolism can have profound effects on health and disease and where it might be a promising target to treat a variety of pathologies is discussed.
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The pharmacology of second-generation chimeric antigen receptors

TL;DR: Current data indicate that CD28-based CARs direct a brisk proliferative response and boost effector functions, whereas 4-1BB-basedCARs induce a more progressive T cell accumulation that may compensate for less immediate potency.
References
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Journal ArticleDOI

mTOR: from growth signal integration to cancer, diabetes and ageing

TL;DR: Mammalian TOR complex 1 (mTORC1) and mTORC2 exert their actions by regulating other important kinases, such as S6 kinase (S6K) and Akt.
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AMPK phosphorylation of raptor mediates a metabolic checkpoint.

TL;DR: AMPK directly phosphorylates the mTOR binding partner raptor on two well-conserved serine residues, and this phosphorylation induces 14-3-3 binding to raptor, uncovering a conserved effector of AMPK that mediates its role as a metabolic checkpoint coordinating cell growth with energy status.
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Differentiation of Effector CD4 T Cell Populations

TL;DR: This review summarizes the discovery, functions, and relationships among Th cells; the cytokine and signaling requirements for their development; the networks of transcription factors involved in their differentiation; the epigenetic regulation of their key cytokines and transcription factors; and human diseases involving defective CD4 T cell differentiation.
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The transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation

TL;DR: Metabolic tracer analysis revealed a Myc-dependent metabolic pathway linking glutaminolysis to the biosynthesis of polyamines, which may represent a general mechanism for metabolic reprogramming under patho-physiological conditions.
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