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Article ; Online: La phagocytose associée à LC3 (LAP) - Phagocytose ou autophagie ?

Galais, Mathilde / Pradel, Baptiste / Vergne, Isabelle / Robert-Hebmann, Véronique / Espert, Lucile / Biard-Piechaczyk, Martine

Medecine sciences : M/S

2019 Volume 35, Issue 8-9, Page(s) 635–642

Abstract: Phagocytosis and macroautophagy, named here autophagy, are two essential mechanisms of lysosomal degradation of diverse cargos into membrane structures. Both mechanisms are involved in immune regulation and cell survival. However, phagocytosis triggers ... ...

Title translation	LAP (LC3-associated phagocytosis): phagocytosis or autophagy?
Abstract	Phagocytosis and macroautophagy, named here autophagy, are two essential mechanisms of lysosomal degradation of diverse cargos into membrane structures. Both mechanisms are involved in immune regulation and cell survival. However, phagocytosis triggers degradation of extracellular material whereas autophagy engulfs only cytoplasmic elements. Furthermore, activation and maturation of these two processes are different. LAP (LC3-associated phagocytosis) is a form of phagocytosis that uses components of the autophagy pathway. It can eliminate (i) pathogens, (ii) immune complexes, (iii) threatening neighbouring cells, dead or alive, and (iv) cell debris, such as POS (photoreceptor outer segment) and the midbody released at the end of mitosis. Cells have thus optimized their means of elimination of dangerous components by sharing some fundamental elements coming from the two main lysosomal degradation pathways.
MeSH term(s)	Animals ; Autophagy/physiology ; Humans ; Immune Evasion/physiology ; Infections/immunology ; Infections/metabolism ; Infections/pathology ; Macrophages/immunology ; Microtubule-Associated Proteins/physiology ; Phagocytosis/physiology ; Phagosomes/immunology
Chemical Substances	MAP1LC3A protein, human ; Microtubule-Associated Proteins
Language	French
Publishing date	2019-09-18
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/2019129
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Article ; Online: HIV-1 Env induces pexophagy and an oxidative stress leading to uninfected CD4

Daussy, Coralie F / Galais, Mathilde / Pradel, Baptiste / Robert-Hebmann, Véronique / Sagnier, Sophie / Pattingre, Sophie / Biard-Piechaczyk, Martine / Espert, Lucile

Autophagy

2020 Volume 17, Issue 9, Page(s) 2465–2474

Abstract: The immunodeficiency observed in HIV-1-infected patients is mainly due to uninfected bystander ... ...

Abstract	The immunodeficiency observed in HIV-1-infected patients is mainly due to uninfected bystander CD4
MeSH term(s)	Autophagy ; CD4-Positive T-Lymphocytes ; Cell Death ; HIV-1 ; Humans ; Macroautophagy ; Oxidative Stress ; T-Lymphocytes
Language	English
Publishing date	2020-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2020.1831814
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Article: Autophagy in HIV-induced T cell death.

Espert, Lucile / Biard-Piechaczyk, Martine

Current topics in microbiology and immunology

2009 Volume 335, Page(s) 307–321

Abstract: HIV infection leads to progressive CD4 T cell depletion, resulting in the development of AIDS. The mechanisms that trigger T cell death after HIV infection are still not fully understood, but a lot of data indicate that apoptosis of uninfected CD4 ... ...

Abstract	HIV infection leads to progressive CD4 T cell depletion, resulting in the development of AIDS. The mechanisms that trigger T cell death after HIV infection are still not fully understood, but a lot of data indicate that apoptosis of uninfected CD4 lymphocytes plays a major role. HIV directly modulates cell death using various strategies in which several viral proteins, in particular the envelope glycoproteins (Env), play an essential role. Importantly, Env, expressed on infected cells, triggers autophagy in uninfected CD4 T cells, leading to their apoptosis. Furthermore, HIV, like other viruses, has evolved strategies to inhibit this autophagic process in HIV-infected cells. This discovery further increases the level of complexity of the cellular processes involved in HIV-induced pathology. Interestingly, HIV protease inhibitors, currently used in highly active antiretroviral therapy (HAART), are able to induce autophagy in cancer cells, leading to a recent repositioning of these drugs as anticancer agents. This review presents an overview of the relationship between HIV, HAART, and autophagy.
MeSH term(s)	Acquired Immunodeficiency Syndrome/drug therapy ; Acquired Immunodeficiency Syndrome/immunology ; Acquired Immunodeficiency Syndrome/virology ; Antiretroviral Therapy, Highly Active ; Autophagy/drug effects ; Autophagy/immunology ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/virology ; HIV Protease Inhibitors/pharmacology ; HIV-1/immunology ; HIV-2/immunology ; Host-Pathogen Interactions/immunology ; Humans ; env Gene Products, Human Immunodeficiency Virus/immunology ; env Gene Products, Human Immunodeficiency Virus/metabolism
Chemical Substances	HIV Protease Inhibitors ; env Gene Products, Human Immunodeficiency Virus
Language	English
Publishing date	2009
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	0070-217X
ISSN	0070-217X
DOI	10.1007/978-3-642-00302-8_15
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Article ; Online: HIV-1 Vpr inhibits autophagy during the early steps of infection of CD4 T cells.

Alfaisal, Jamal / Machado, Alice / Galais, Mathilde / Robert-Hebmann, Véronique / Arnauné-Pelloquin, Laetitia / Espert, Lucile / Biard-Piechaczyk, Martine

Biology of the cell

2019 Volume 111, Issue 12, Page(s) 308–318

Abstract: Background information: Autophagy is induced during HIV-1 entry into CD4 T cells by the fusion of the membranes triggered by the gp41 envelope glycoprotein. This anti-HIV-1 mechanism is inhibited by the viral infectivity factor (Vif) neosynthesized ... ...

Abstract	Background information: Autophagy is induced during HIV-1 entry into CD4 T cells by the fusion of the membranes triggered by the gp41 envelope glycoprotein. This anti-HIV-1 mechanism is inhibited by the viral infectivity factor (Vif) neosynthesized after HIV-1 integration to allow viral replication. However, autophagy is very rapidly controlled after HIV-1 entry by a still unknown mechanism. As HIV-1 viral protein R (Vpr) is the only auxiliary protein found within the virion in substantial amount, we studied its capability to control the early steps of HIV-1 envelope-mediated autophagy. Results: We demonstrated that ectopic Vpr inhibits autophagy in both the Jurkat CD4 T cell line and HEK.293T cells. Interestingly, Vpr coming from the virus also blocks autophagy in CD4 T cells, the main cell target of HIV-1. Furthermore, Vpr decreases the expression level of two essential autophagy proteins (ATG), LC3B and Beclin-1, and an important autophagy-related protein, BNIP3 as well as the level of their mRNA. We also demonstrated in HEK.293T cells that Vpr degrades the FOXO3a transcription factor through the ubiquitin proteasome system. Conclusion: Vpr, the only well-expressed HIV-1 auxiliary protein incorporated into viruses, is able to negatively control autophagy induced during HIV-1 entry into CD4 T cells. Significance: We provide insights of how HIV-1 controls autophagy very early after its entry into CD4 T cells and discovered a new function of Vpr. These results open the route to a better understanding of the roles of Vpr during HIV-1 infection through FOXO3a degradation and could be important to consider additional therapies that counteract the role of Vpr on autophagy.
MeSH term(s)	Autophagy/immunology ; Beclin-1/immunology ; CD4-Positive T-Lymphocytes/cytology ; CD4-Positive T-Lymphocytes/immunology ; HEK293 Cells ; HIV Infections/immunology ; HIV-1/immunology ; HIV-1/physiology ; Humans ; Jurkat Cells ; Membrane Proteins/immunology ; Microtubule-Associated Proteins/immunology ; Proto-Oncogene Proteins/immunology ; Tumor Suppressor Proteins/immunology ; Virus Replication ; vpr Gene Products, Human Immunodeficiency Virus/immunology
Chemical Substances	BECN1 protein, human ; BNIP3L protein, human ; Beclin-1 ; MAP1LC3B protein, human ; Membrane Proteins ; Microtubule-Associated Proteins ; Proto-Oncogene Proteins ; Tumor Suppressor Proteins ; vpr Gene Products, Human Immunodeficiency Virus ; vpr protein, Human immunodeficiency virus 1
Language	English
Publishing date	2019-10-30
Publishing country	England
Document type	Journal Article
ZDB-ID	245745-3
ISSN	1768-322X ; 0399-0311 ; 0248-4900
ISSN (online)	1768-322X
ISSN	0399-0311 ; 0248-4900
DOI	10.1111/boc.201900071
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Article ; Online: Autophagie, protéines ATG et maladies infectieuses.

Vergne, Isabelle / Lafont, Frank / Espert, Lucile / Esclatine, Audrey / Biard-Piechaczyk, Martine

Medecine sciences : M/S

2017 Volume 33, Issue 3, Page(s) 312–318

Abstract: One of the main functions of the autophagy pathway is to control infections. Intracellular micro-organisms or their products once internalized in the host cell can be directly degraded by autophagy, a process called xenophagy. Autophagy is also involved ... ...

Title translation	Autophagy, ATG proteins and infectious diseases.
Abstract	One of the main functions of the autophagy pathway is to control infections. Intracellular micro-organisms or their products once internalized in the host cell can be directly degraded by autophagy, a process called xenophagy. Autophagy is also involved in other innate immune responses and participates to the adaptive immune system. In addition, several autophagy proteins play a role in the development of infectious diseases independently of their role in the autophagy pathway. To replicate efficiently, pathogens have therefore evolved to counteract this process or to exploit it to their own profit. The review focuses on the relationship between autophagy and micro-organisms, which is highly diverse and complex. Many research groups are now working on this topic to find new therapeutics and/or vaccines. Given the large number of data, we have addressed this subject through some representative examples.
MeSH term(s)	Animals ; Autophagy/physiology ; Autophagy-Related Proteins/physiology ; Communicable Diseases/immunology ; Communicable Diseases/pathology ; Host-Pathogen Interactions/immunology ; Humans ; Immunity, Innate/physiology
Chemical Substances	Autophagy-Related Proteins
Language	French
Publishing date	2017-03
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/20173303019
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Article ; Online: Macroautophagy Regulation during HIV-1 Infection of CD4+ T Cells and Macrophages.

Borel, Sophie / Espert, Lucile / Biard-Piechaczyk, Martine

Frontiers in immunology

2012 Volume 3, Page(s) 97

Abstract: Autophagy is an intracellular mechanism whereby pathogens, particularly viruses, are destroyed in autolysosomes after their entry into targets cells. Therefore, to survive and replicate in host cells, viruses have developed multiple strategies to either ... ...

Abstract	Autophagy is an intracellular mechanism whereby pathogens, particularly viruses, are destroyed in autolysosomes after their entry into targets cells. Therefore, to survive and replicate in host cells, viruses have developed multiple strategies to either counteract or exploit this process. The aim of this review is to outline the known relationships between HIV-1 and autophagy in CD4+ T lymphocytes and macrophages, two main HIV-1 cell targets. The differential regulation of autophagy in these two cell-types is highlighted and its potential consequences in terms of viral replication and physiopathology discussed.
Language	English
Publishing date	2012-05-07
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.2012.00097
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Article ; Online: Brief Report: Impaired CD4 T-Cell Response to Autophagy in Treated HIV-1-Infected Individuals.

Gómez-Mora, Elisabet / Robert-Hebmann, Véronique / García, Elisabet / Massanella, Marta / Clotet, Bonaventura / Cabrera, Cecilia / Blanco, Julià / Biard-Piechaczyk, Martine

Journal of acquired immune deficiency syndromes (1999)

2016 Volume 74, Issue 2, Page(s) 201–205

Abstract: Autophagy restricts infection of CD4 T lymphocytes by HIV-1, but little is known about autophagy in treated HIV-1-infected individuals. We have analyzed the capability of CD4 T cells from aviremic-treated individuals to trigger autophagy and correlated ... ...

Abstract	Autophagy restricts infection of CD4 T lymphocytes by HIV-1, but little is known about autophagy in treated HIV-1-infected individuals. We have analyzed the capability of CD4 T cells from aviremic-treated individuals to trigger autophagy and correlated this response with parameters known to be important for immunological recovery. Autophagy was significantly decreased in CD4 T cells from HIV-1-treated individuals compared with uninfected controls, and this defective autophagic response was more pronounced in individuals with poor CD4 T-cell recovery, suggesting a link between impaired autophagy in CD4 T cells and chronic immunological defects that remain in treated HIV infection.
MeSH term(s)	Adult ; Anti-Retroviral Agents/therapeutic use ; Autophagy ; CD4-Positive T-Lymphocytes/immunology ; Cross-Sectional Studies ; Female ; HIV Infections/drug therapy ; HIV Infections/immunology ; HIV Infections/pathology ; HIV Infections/virology ; HIV-1/immunology ; Humans ; Male ; Middle Aged ; Pilot Projects
Chemical Substances	Anti-Retroviral Agents
Language	English
Publishing date	2016-10-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	645053-2
ISSN	1944-7884 ; 1077-9450 ; 0897-5965 ; 0894-9255 ; 1525-4135
ISSN (online)	1944-7884 ; 1077-9450
ISSN	0897-5965 ; 0894-9255 ; 1525-4135
DOI	10.1097/QAI.0000000000001201
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Article: Involvement of autophagy in viral infections: antiviral function and subversion by viruses.

Espert, Lucile / Codogno, Patrice / Biard-Piechaczyk, Martine

Journal of molecular medicine (Berlin, Germany)

2007 Volume 85, Issue 8, Page(s) 811–823

Abstract: Autophagy is a cellular process involved in the degradation and turn-over of long-lived proteins and organelles, which can be subjected to suppression or further induction in response to different stimuli. According to its essential role in cellular ... ...

Abstract	Autophagy is a cellular process involved in the degradation and turn-over of long-lived proteins and organelles, which can be subjected to suppression or further induction in response to different stimuli. According to its essential role in cellular homeostasis, autophagy has been implicated in several pathologies including cancer, neurodegeneration and myopathies. More recently, autophagy has been described as a mechanism of both innate and adaptive immunity against intracellular bacteria and viruses. In this context, autophagy has been proposed as a protective mechanism against viral infection by degrading the pathogens into autolysosomes. This is strengthened by the fact that several proteins involved in interferon (IFN) signalling pathways are linked to autophagy regulation. However, several viruses have evolved strategies to divert IFN-mediated pathways and autophagy to their own benefit. This review provides an overview of the autophagic process and its involvement in the infection by different viral pathogens and of the connections existing between autophagy and proteins involved in IFN signalling pathways.
MeSH term(s)	Animals ; Autophagy/immunology ; Autophagy/physiology ; Humans ; Immunity, Innate/immunology ; Interferons/immunology ; Interferons/metabolism ; Interferons/physiology ; Signal Transduction/immunology ; Virus Diseases/immunology ; Virus Diseases/virology ; Viruses/immunology
Chemical Substances	Interferons (9008-11-1)
Keywords	covid19
Language	English
Publishing date	2007-03-06
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1223802-8
ISSN	1432-1440 ; 0946-2716
ISSN (online)	1432-1440
ISSN	0946-2716
DOI	10.1007/s00109-007-0173-6
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Article ; Online: What is the role of autophagy in HIV-1 infection?

Espert, Lucile / Codogno, Patrice / Biard-Piechaczyk, Martine

Autophagy

2007 Volume 4, Issue 3, Page(s) 273–275

Abstract: HIV-1 infection is characterized by a progressive CD4 T cell depletion. It is now accepted that apoptosis of uninfected bystander CD4 T lymphocytes plays a major role in AIDS development. Viral envelope glycoproteins (Env) are mainly involved in inducing ...

Abstract	HIV-1 infection is characterized by a progressive CD4 T cell depletion. It is now accepted that apoptosis of uninfected bystander CD4 T lymphocytes plays a major role in AIDS development. Viral envelope glycoproteins (Env) are mainly involved in inducing this cell death process, but the mechanisms triggered by HIV-1 leading to immunodeficiency are still poorly understood. Recently, we have demonstrated that autophagy is a prerequisite for Env-mediated apoptosis in uninfected CD4 T cells, underlining its role in HIV-1 infection. However, occurrence of autophagy in HIV-1-infected cells has not yet been described. Several hypotheses are discussed, based on the comparison with data from other viral infections.
MeSH term(s)	Animals ; Apoptosis/physiology ; Autophagy/physiology ; CD4-Positive T-Lymphocytes/pathology ; CD4-Positive T-Lymphocytes/virology ; HIV Infections/metabolism ; HIV Infections/pathology ; HIV Infections/virology ; HIV-1/physiology ; env Gene Products, Human Immunodeficiency Virus/physiology
Chemical Substances	env Gene Products, Human Immunodeficiency Virus
Keywords	covid19
Language	English
Publishing date	2007-10-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.4161/auto.5211
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Article ; Online: Inhibition of HIV-1 replication with stable RNAi-mediated knockdown of autophagy factors.

Eekels, Julia Jm / Sagnier, Sophie / Geerts, Dirk / Jeeninga, Rienk E / Biard-Piechaczyk, Martine / Berkhout, Ben

Virology journal

2012 Volume 9, Page(s) 69

Abstract: Autophagy is a cellular process leading to the degradation of cytoplasmic components such as organelles and intracellular pathogens. It has been shown that HIV-1 relies on several components of the autophagy pathway for its replication, but the virus ... ...

Abstract	Autophagy is a cellular process leading to the degradation of cytoplasmic components such as organelles and intracellular pathogens. It has been shown that HIV-1 relies on several components of the autophagy pathway for its replication, but the virus also blocks late steps of autophagy to prevent its degradation. We generated stable knockdown T cell lines for 12 autophagy factors and analyzed the impact on HIV-1 replication. RNAi-mediated knockdown of 5 autophagy factors resulted in inhibition of HIV-1 replication. Autophagy analysis confirmed a specific defect in the autophagy pathway for 4 of these 5 factors. We also scored the impact on cell viability, but no gross effects were observed. Upon simultaneous knockdown of 2 autophagy factors (Atg16 and Atg5), an additive inhibitory effect was scored on HIV-1 replication. Stable knockdown of several autophagy factors inhibit HIV-1 replication without any apparent cytotoxicity. We therefore propose that targeting of the autophagy pathway can be a novel therapeutic approach against HIV-1.
MeSH term(s)	Autophagy ; Cell Line ; Cell Survival ; Gene Knockdown Techniques ; HIV-1/growth & development ; HIV-1/physiology ; Humans ; T-Lymphocytes/virology ; Virus Replication
Language	English
Publishing date	2012-03-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1743-422X
ISSN (online)	1743-422X
DOI	10.1186/1743-422X-9-69
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