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Article: Class I PI3K Provide Lipid Substrate in T Cell Autophagy Through Linked Activity of Inositol Phosphatases.

McLeod, Ian X / Saxena, Ruchi / Carico, Zachary / He, You-Wen

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 709398

Abstract: Autophagy, a highly conserved intracellular process, has been identified as a novel mechanism regulating T lymphocyte homeostasis. Herein, we demonstrate that both starvation- and T cell receptor-mediated autophagy induction requires class I ... ...

Abstract	Autophagy, a highly conserved intracellular process, has been identified as a novel mechanism regulating T lymphocyte homeostasis. Herein, we demonstrate that both starvation- and T cell receptor-mediated autophagy induction requires class I phosphatidylinositol-3 kinases to produce PI(3)P. In contrast, common gamma chain cytokines are suppressors of autophagy despite their ability to activate the PI3K pathway. T cells lacking the PI3KI regulatory subunits, p85 and p55, were almost completely unable to activate TCR-mediated autophagy and had concurrent defects in PI(3)P production. Additionally, T lymphocytes upregulate polyinositol phosphatases in response to autophagic stimuli, and the activity of the inositol phosphatases Inpp4 and SHIP are required for TCR-mediated autophagy induction. Addition of exogenous PI(3,4)P
Language	English
Publishing date	2021-08-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.709398
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Article ; Online: Class I PI3K Provide Lipid Substrate in T Cell Autophagy Through Linked Activity of Inositol Phosphatases

Ian X. McLeod / Ruchi Saxena / Zachary Carico / You-Wen He

Frontiers in Cell and Developmental Biology, Vol

2021 Volume 9

Abstract	Autophagy, a highly conserved intracellular process, has been identified as a novel mechanism regulating T lymphocyte homeostasis. Herein, we demonstrate that both starvation- and T cell receptor-mediated autophagy induction requires class I phosphatidylinositol-3 kinases to produce PI(3)P. In contrast, common gamma chain cytokines are suppressors of autophagy despite their ability to activate the PI3K pathway. T cells lacking the PI3KI regulatory subunits, p85 and p55, were almost completely unable to activate TCR-mediated autophagy and had concurrent defects in PI(3)P production. Additionally, T lymphocytes upregulate polyinositol phosphatases in response to autophagic stimuli, and the activity of the inositol phosphatases Inpp4 and SHIP are required for TCR-mediated autophagy induction. Addition of exogenous PI(3,4)P2 can supplement cellular PI(3)P and accelerate the outcome of activation-induced autophagy. TCR-mediated autophagy also requires internalization of the TCR complex, suggesting that this kinase/phosphatase activity is localized in internalized vesicles. Finally, HIV-induced bystander CD4+ T cell autophagy is dependent upon PI3KI. Overall, our data elucidate an important pathway linking TCR activation to autophagy, via induction of PI3KI activity and inositol phosphatase upregulation to produce PI(3)P.
Keywords	autophagy ; PI3K I ; T cells ; lipid kinase ; lipid phosphatase ; cytokines ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2021-08-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article ; Online: Editorial: TRPV1: how thymocytes sense stress and respond with autophagy.

McLeod, Ian X / He, You-Wen

Journal of leukocyte biology

2012 Volume 92, Issue 3, Page(s) 409–411

MeSH term(s)	Animals ; Autophagy/immunology ; Autophagy-Related Proteins ; Cysteine Endopeptidases/metabolism ; Male ; Protein Kinases/metabolism ; Reactive Oxygen Species/metabolism ; TRPV Cation Channels/metabolism ; Thymocytes/metabolism
Chemical Substances	Autophagy-Related Proteins ; Reactive Oxygen Species ; TRPV Cation Channels ; TRPV1 protein, mouse ; Protein Kinases (EC 2.7.-) ; AMP-activated protein kinase kinase (EC 2.7.1.-) ; Atg4C protein, mouse (EC 3.4.22.-) ; Cysteine Endopeptidases (EC 3.4.22.-)
Language	English
Publishing date	2012-08-30
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1189/jlb.0612269
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Article ; Online: The contribution of autophagy to lymphocyte survival and homeostasis.

McLeod, Ian X / Jia, Wei / He, You-Wen

Immunological reviews

2012 Volume 249, Issue 1, Page(s) 195–204

Abstract: Over the life span of a T lymphocyte, from thymic development to death, it is subjected to a variety of stresses and stimuli. Upon receipt of each stress or stimulus, a potentially life-changing fate decision must be made, namely, whether to commit to a ... ...

Abstract	Over the life span of a T lymphocyte, from thymic development to death, it is subjected to a variety of stresses and stimuli. Upon receipt of each stress or stimulus, a potentially life-changing fate decision must be made, namely, whether to commit to a form of programmed cell death or to make the necessary adaptations to effectively deal with the changing environment. In our laboratory, we have identified several stresses that a T lymphocyte will encounter during a normal life span. Our studies have focused on how T cells utilize autophagy to get a grasp on the situation, or in cases in which survival is untenable, how T cells use autophagy to hasten their demise. This review focuses on the functions of T-cell autophagy in maintaining homeostasis, eliminating excess or dangerous levels of mitochondria, trimming levels of endoplasmic reticulum, and promoting a healthy metabolic level to allow cells to perform as productive components of the immune system. In addition, the use of autophagy signaling molecules to perform autophagy-independent tasks involved in the maintenance of immune homeostasis is discussed.
MeSH term(s)	Animals ; Autophagy ; B-Lymphocytes/cytology ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; B-Lymphocytes/physiology ; Endoplasmic Reticulum/metabolism ; Energy Metabolism ; Homeostasis ; Humans ; Mitochondria/metabolism ; Signal Transduction ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; T-Lymphocytes/physiology
Language	English
Publishing date	2012-08-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/j.1600-065X.2012.01143.x
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Article ; Online: Roles of autophagy in lymphocytes: reflections and directions.

McLeod, Ian X / He, Youwen

Cellular & molecular immunology

2010 Volume 7, Issue 2, Page(s) 104–107

Abstract: Recent studies have revealed that autophagy, a fundamental intracellular process, plays many different roles in lymphocyte development and function. Autophagy regulates naive T-lymphocyte homeostasis, specifically by regulating mitochondrial quality and ... ...

Abstract	Recent studies have revealed that autophagy, a fundamental intracellular process, plays many different roles in lymphocyte development and function. Autophagy regulates naive T-lymphocyte homeostasis, specifically by regulating mitochondrial quality and turnover, and is necessary for the proliferation of mature T cells. Autophagy also acts as a cellular death pathway in lymphocytes, both upon prolonged cytokine withdrawal and during acute antigen-receptor stimulation if improperly regulated. Furthermore, during HIV infection, hyperinduction of autophagy leads to massive T-cell death in uninfected CD4(+) T cells, and is rescued by inhibiting autophagic initiation. Constitutively high levels of autophagy in thymic epithelial cells are necessary for optimal processing and presentation of endogenous antigens, and required for proper positive and negative selection of developing thymocytes. Autophagy also promotes the survival of B lymphocytes, as well as the development of early B-cell progenitors. In B cells, autophagy is an alternative death pathway, as antigen-receptor stimulation in the absence of costimulation induces a potent autophagic death. Thus, autophagy plays a complex role in lymphocytes and is regulated during their lifespan to ensure a healthy immune system.
MeSH term(s)	Animals ; Autophagy ; B-Lymphocytes/cytology ; B-Lymphocytes/immunology ; Homeostasis ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology ; Thymus Gland/immunology
Language	English
Publishing date	2010-02-01
Publishing country	China
Document type	Journal Article ; Review
ZDB-ID	2435097-7
ISSN	2042-0226 ; 1672-7681
ISSN (online)	2042-0226
ISSN	1672-7681
DOI	10.1038/cmi.2009.115
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Article: Autophagy, a novel pathway to regulate calcium mobilization in T lymphocytes.

Jia, Wei / He, Ming-Xiao / McLeod, Ian X / He, You-Wen

Frontiers in immunology

2013 Volume 4, Page(s) 179

Abstract: The T lymphocyte response initiates with the recognition of MHC/peptides on antigen presenting cells by the T cell receptor (TCR). After the TCR engagement, the proximal signaling pathways are activated for downstream cellular events. Among these ... ...

Abstract	The T lymphocyte response initiates with the recognition of MHC/peptides on antigen presenting cells by the T cell receptor (TCR). After the TCR engagement, the proximal signaling pathways are activated for downstream cellular events. Among these pathways, the calcium-signaling flux is activated through the depletion of endoplasmic reticulum (ER) calcium stores and plays pivotal roles in T cell proliferation, cell survival, and apoptosis. In studying the roles of macroautophagy (hereafter referred to as autophagy) in T cell function, we found that a pathway for intracellular degradation, autophagy, regulates calcium signaling by developmentally maintaining the homeostasis of the ER. Using mouse genetic models with specific deletion of autophagy-related genes in T lymphocytes, we found that the calcium influx is defective and the calcium efflux is increased in autophagy-deficient T cells. The abnormal calcium flux is related to the expansion of the ER and higher calcium stores in the ER. Because of this, treatment with the ER sarco/ER Ca(2+)-ATPase pump inhibitor, thapsigargin, rescues the calcium influx defect in autophagy-deficient T cells. Therefore, autophagy regulates calcium mobilization in T lymphocytes through ER homeostasis.
Language	English
Publishing date	2013-07-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2013.00179
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Article ; Online: Autophagy regulates T lymphocyte proliferation through selective degradation of the cell-cycle inhibitor CDKN1B/p27Kip1.

Jia, Wei / He, Ming-Xiao / McLeod, Ian X / Guo, Jian / Ji, Dong / He, You-Wen

Autophagy

2015 Volume 11, Issue 12, Page(s) 2335–2345

Abstract: The highly conserved cellular degradation pathway, macroautophagy, regulates the homeostasis of organelles and promotes the survival of T lymphocytes. Previous results indicate that Atg3-, Atg5-, or Pik3c3/Vps34-deficient T cells cannot proliferate ... ...

Abstract	The highly conserved cellular degradation pathway, macroautophagy, regulates the homeostasis of organelles and promotes the survival of T lymphocytes. Previous results indicate that Atg3-, Atg5-, or Pik3c3/Vps34-deficient T cells cannot proliferate efficiently. Here we demonstrate that the proliferation of Atg7-deficient T cells is defective. By using an adoptive transfer and Listeria monocytogenes (LM) mouse infection model, we found that the primary immune response against LM is intrinsically impaired in autophagy-deficient CD8(+) T cells because the cell population cannot expand after infection. Autophagy-deficient T cells fail to enter into S-phase after TCR stimulation. The major negative regulator of the cell cycle in T lymphocytes, CDKN1B, is accumulated in autophagy-deficient naïve T cells and CDKN1B cannot be degraded after TCR stimulation. Furthermore, our results indicate that genetic deletion of one allele of CDKN1B in autophagy-deficient T cells restores proliferative capability and the cells can enter into S-phase after TCR stimulation. Finally, we found that natural CDKN1B forms polymers and is physiologically associated with the autophagy receptor protein SQSTM1/p62 (sequestosome 1). Collectively, autophagy is required for maintaining the expression level of CDKN1B in naïve T cells and selectively degrades CDKN1B after TCR stimulation.
MeSH term(s)	Animals ; Autophagy/physiology ; Cell Cycle Checkpoints/physiology ; Cell Proliferation/physiology ; Cyclin-Dependent Kinase Inhibitor p27/genetics ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Homeostasis/physiology ; Lymphocyte Activation/immunology ; Mice ; Mice, Transgenic ; Microtubule-Associated Proteins/metabolism ; Mitochondria/metabolism ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology
Chemical Substances	Cdkn1b protein, mouse ; Microtubule-Associated Proteins ; Cyclin-Dependent Kinase Inhibitor p27 (147604-94-2)
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2015.1110666
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Article ; Online: Macroautophagy in T lymphocyte development and function.

He, Ming-Xiao / McLeod, Ian X / Jia, Wei / He, You-Wen

Frontiers in immunology

2012 Volume 3, Page(s) 22

Abstract: Macroautophagy (referred to as autophagy) is a fundamental intracellular process characterized by the sequestration of cytoplasmic compartments through double-membrane vesicles, termed autophagosomes. Recent studies have established important roles of ... ...

Abstract	Macroautophagy (referred to as autophagy) is a fundamental intracellular process characterized by the sequestration of cytoplasmic compartments through double-membrane vesicles, termed autophagosomes. Recent studies have established important roles of autophagy in regulating T lymphocyte development and function. Resting T lymphocytes have basal levels of autophagy that is upregulated by T cell receptor stimulation. Several specific knockout or transgenic models have been developed during the past few years, and it has been revealed that autophagy plays an essential role in regulating thymocyte selection, peripheral T cell survival, and proliferation. The regulation of T cell development and function by autophagy is mediated through its role in regulating self-antigen presentation, intracellular organelle homeostasis, and energy production. Here we will review the current findings concerning how autophagy regulates T cell function, as well as compare different models in studying autophagy in T lymphocytes.
Language	English
Publishing date	2012-02-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2012.00022
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Article ; Online: The class III kinase Vps34 promotes T lymphocyte survival through regulating IL-7Rα surface expression.

McLeod, Ian X / Zhou, Xiang / Li, Qi-Jing / Wang, Fan / He, You-Wen

Journal of immunology (Baltimore, Md. : 1950)

2011 Volume 187, Issue 10, Page(s) 5051–5061

Abstract: IL-7Rα-mediated signals are essential for naive T lymphocyte survival. Recent studies show that IL-7Rα is internalized and either recycled to cell surface or degraded. However, how the intracellular process of IL-7Rα trafficking is regulated is unclear. ... ...

Abstract	IL-7Rα-mediated signals are essential for naive T lymphocyte survival. Recent studies show that IL-7Rα is internalized and either recycled to cell surface or degraded. However, how the intracellular process of IL-7Rα trafficking is regulated is unclear. In this paper, we show that Vps34, the class III PI3K, plays a critical role in proper IL-7Rα intracellular trafficking. Mice lacking Vps34 in T lymphocytes had a severely reduced T lymphocyte compartment. Vps34-deficient T lymphocytes exhibit increased death and reduced IL-7Rα surface expression, although three major forms of autophagy remain intact. Intracellular IL-7Rα in normal T lymphocytes at steady state is trafficked through either early endosome/multivesicular bodies to the late endosome-Golgi for surface expression or to the lysosome for degradation. However, Vps34-deficient T cells have mislocalized intracellular Eea1, HGF-regulated tyrosine kinase substrate, and Vps36 protein levels, the combined consequence of which is the inability to mobilize internalized IL-7Rα into the retromer pathway for surface display. Our studies reveal that Vps34, though dispensable for autophagy induction, is a critical regulator of naive T cell homeostasis, modulating IL-7Rα trafficking, signaling, and recycling.
MeSH term(s)	Animals ; Apoptosis Regulatory Proteins/deficiency ; Apoptosis Regulatory Proteins/genetics ; Autophagy/genetics ; Autophagy/immunology ; Bcl-2-Like Protein 11 ; Cell Cycle/genetics ; Cell Cycle/immunology ; Cell Survival/genetics ; Cell Survival/immunology ; Class III Phosphatidylinositol 3-Kinases/physiology ; Gene Expression Regulation/immunology ; Homeostasis/genetics ; Homeostasis/immunology ; Membrane Proteins/biosynthesis ; Membrane Proteins/deficiency ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; Mice, Transgenic ; Protein Transport/genetics ; Protein Transport/immunology ; Proto-Oncogene Proteins/deficiency ; Proto-Oncogene Proteins/genetics ; Receptors, Interleukin-7/biosynthesis ; Receptors, Interleukin-7/genetics ; Receptors, Interleukin-7/metabolism ; Signal Transduction/genetics ; Signal Transduction/immunology ; T-Lymphocyte Subsets/cytology ; T-Lymphocyte Subsets/enzymology ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/enzymology ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	Apoptosis Regulatory Proteins ; Bcl-2-Like Protein 11 ; Bcl2l11 protein, mouse ; Membrane Proteins ; Proto-Oncogene Proteins ; Receptors, Interleukin-7 ; interleukin-7 receptor, alpha chain ; Class III Phosphatidylinositol 3-Kinases (EC 2.7.1.137)
Language	English
Publishing date	2011-10-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1100710
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Article ; Online: APC16 is a conserved subunit of the anaphase-promoting complex/cyclosome.

Kops, Geert J P L / van der Voet, Monique / Manak, Michael S / van Osch, Maria H J / Naini, Said Movahedi / Brear, Andrea / McLeod, Ian X / Hentschel, Dirk M / Yates, John R / van den Heuvel, Sander / Shah, Jagesh V

Journal of cell science

2015 Volume 128, Issue 21, Page(s) 4025

Language	English
Publishing date	2015-10-22
Publishing country	England
Document type	Published Erratum
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.180935
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