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  1. Article ; Online: Lose appetite, lose control: integrins and noncanonical autophagy regulate germinal center reactions.

    Leventhal, Jeremy S

    The Journal of clinical investigation

    2018  Volume 128, Issue 9, Page(s) 3752–3753

    Abstract: T cell-dependent germinal center (GC) reactions are the pinnacle of adaptive immune responses, with profound effects on human health and disease. It has long been known that ligands of an innate immune pattern recognition receptor subgroup, TLRs, amplify ...

    Abstract T cell-dependent germinal center (GC) reactions are the pinnacle of adaptive immune responses, with profound effects on human health and disease. It has long been known that ligands of an innate immune pattern recognition receptor subgroup, TLRs, amplify antibody responses; however, the mechanisms regulating this phenomenon are poorly understood. In this issue of the JCI, Raso et al. demonstrate that αvβ3 integrins regulate the magnitude and speed of TLR-augmented GC reactions, limiting both short- and long-term humoral immunity. This phenomenon is dependent on a noncanonical form of the autophagy pathway and Rubicon, a noncanonical autophagy-associated protein. B cell-specific deletion of the gene encoding αvβ3 integrin enhanced GC responses in mice and conferred a dramatic survival advantage compared with controls after influenza infection, confirming that B cell integrin manipulation represents a potential and exciting target for augmenting or inhibiting GC reactions.
    MeSH term(s) Animals ; Appetite ; Autophagy ; B-Lymphocytes ; Germinal Center ; Humans ; Integrin alphaV ; Integrins ; Mice
    Chemical Substances Integrin alphaV ; Integrins
    Language English
    Publishing date 2018-08-20
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI122766
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  2. Article ; Online: Hypertension and glomerular diseases: the importance of a holistic approach.

    Cravedi, Paolo / Leventhal, Jeremy S / Piccoli, Giorgina B

    Journal of nephrology

    2021  Volume 34, Issue 4, Page(s) 1053–1055

    MeSH term(s) Humans ; Hypertension/diagnosis ; Hypertension/epidemiology ; Kidney Diseases/diagnosis ; Kidney Diseases/therapy
    Language English
    Publishing date 2021-02-12
    Publishing country Italy
    Document type Editorial ; Comment
    ZDB-ID 1093991-x
    ISSN 1724-6059 ; 1120-3625 ; 1121-8428
    ISSN (online) 1724-6059
    ISSN 1120-3625 ; 1121-8428
    DOI 10.1007/s40620-021-00977-4
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    Zs.A 3369: Show issues Location:
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  3. Article ; Online: T Cells and Acute Kidney Injury: A Two-Way Relationship.

    Dellepiane, Sergio / Leventhal, Jeremy S / Cravedi, Paolo

    Frontiers in immunology

    2020  Volume 11, Page(s) 1546

    Abstract: Acute Kidney Injury (AKI) complicates up to 10% of hospital admissions substantially increasing patient morbidity and mortality. Experimental evidence supports that AKI initiation and maintenance results from immune-mediated damage. Exogenous injury ... ...

    Abstract Acute Kidney Injury (AKI) complicates up to 10% of hospital admissions substantially increasing patient morbidity and mortality. Experimental evidence supports that AKI initiation and maintenance results from immune-mediated damage. Exogenous injury sources directly damage renal cells which produce pro-inflammatory mediators recruiting immune cells and furthering kidney injury. Many AKI studies focus on activation of innate immunity; major components include complement pathways, neutrophils, and monocytes. Recently, growing evidence emphasizes T lymphocytes role in affecting AKI pathogenesis and magnitude. In particular, T helper 17 lymphocytes enhance tissue injury by recruiting neutrophils and other inflammatory cells, while regulatory T cells conversely reduce renal injury and facilitate repair. Intriguingly, evidence supports local parenchymal-T cell interactions as essential to producing T cell phenotypic changes affecting long-term kidney and patient survival. Herein, we review T cells effects on AKI and patient outcomes and discuss related new therapeutic approaches to improve outcomes of affected individuals.
    MeSH term(s) Acute Kidney Injury/etiology ; Acute Kidney Injury/metabolism ; Acute Kidney Injury/pathology ; Acute Kidney Injury/therapy ; Adaptive Immunity ; Animals ; Disease Management ; Disease Susceptibility/immunology ; Humans ; Immunity, Innate ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
    Language English
    Publishing date 2020-07-17
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2020.01546
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  4. Article ; Online: Totally tubular, dude: rethinking DKD pathogenesis in the wake of SGLT2i data.

    Yu, Samuel Mon-Wei / Leventhal, Jeremy S / Cravedi, Paolo

    Journal of nephrology

    2020  Volume 34, Issue 3, Page(s) 629–631

    MeSH term(s) Diabetic Nephropathies ; Humans ; Sodium-Glucose Transporter 2 ; Sodium-Glucose Transporter 2 Inhibitors/adverse effects
    Chemical Substances Sodium-Glucose Transporter 2 ; Sodium-Glucose Transporter 2 Inhibitors
    Language English
    Publishing date 2020-09-23
    Publishing country Italy
    Document type Editorial
    ZDB-ID 1093991-x
    ISSN 1724-6059 ; 1120-3625 ; 1121-8428
    ISSN (online) 1724-6059
    ISSN 1120-3625 ; 1121-8428
    DOI 10.1007/s40620-020-00868-0
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    Zs.A 3369: Show issues Location:
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  5. Article ; Online: Membranous nephropathy: setting the bar for hypothesis-driven, selective therapies in nephrology.

    Angeletti, Andrea / Leventhal, Jeremy S / Cravedi, Paolo

    Journal of nephrology

    2020  Volume 34, Issue 2, Page(s) 561–563

    MeSH term(s) Autoantibodies ; Glomerulonephritis, Membranous/diagnosis ; Glomerulonephritis, Membranous/drug therapy ; Humans ; Nephrology ; Receptors, Phospholipase A2 ; Rituximab
    Chemical Substances Autoantibodies ; Receptors, Phospholipase A2 ; Rituximab (4F4X42SYQ6)
    Language English
    Publishing date 2020-08-27
    Publishing country Italy
    Document type Editorial
    ZDB-ID 1093991-x
    ISSN 1724-6059 ; 1120-3625 ; 1121-8428
    ISSN (online) 1724-6059
    ISSN 1120-3625 ; 1121-8428
    DOI 10.1007/s40620-020-00806-0
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  6. Article ; Online: LAPping up dead cells to prevent lupus nephritis: a novel role for noncanonical autophagy in autoimmunity.

    Leventhal, Jeremy S / Ross, Michael J

    Kidney international

    2016  Volume 90, Issue 2, Page(s) 238–239

    Abstract: The mechanisms underlying the development of systemic lupus erythematosus and lupus nephritis remain poorly understood. A recent study demonstrates that deficiencies in the immune system's ability to degrade scavenged dead cells via noncanonical ... ...

    Abstract The mechanisms underlying the development of systemic lupus erythematosus and lupus nephritis remain poorly understood. A recent study demonstrates that deficiencies in the immune system's ability to degrade scavenged dead cells via noncanonical autophagy is sufficient to break immune tolerance and produce features commonly seen in lupus, including circulating autoantibodies, inflammatory cytokines, and nephritis. This work provides a possible mechanism for the association of polymorphisms in autophagy genes with the risk of lupus.
    MeSH term(s) Autoantibodies/immunology ; Autoimmunity/immunology ; Autophagy/genetics ; Humans ; Lupus Erythematosus, Systemic/genetics ; Lupus Nephritis/genetics
    Chemical Substances Autoantibodies
    Language English
    Publishing date 2016-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2016.06.001
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    Zs.A 797: Show issues Location:
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  7. Article: Podocyte Autophagy in Homeostasis and Disease.

    Lin, Qisheng / Banu, Khadija / Ni, Zhaohui / Leventhal, Jeremy S / Menon, Madhav C

    Journal of clinical medicine

    2021  Volume 10, Issue 6

    Abstract: Autophagy is a protective mechanism that removes dysfunctional components and provides nutrition for cells. Podocytes are terminally differentiated specialized epithelial cells that wrap around the capillaries of the glomerular filtration barrier and ... ...

    Abstract Autophagy is a protective mechanism that removes dysfunctional components and provides nutrition for cells. Podocytes are terminally differentiated specialized epithelial cells that wrap around the capillaries of the glomerular filtration barrier and show high autophagy level at the baseline. Here, we provide an overview of cellular autophagy and its regulation in homeostasis with specific reference to podocytes. We discuss recent data that have focused on the functional role and regulation of autophagy during podocyte injury in experimental and clinical glomerular diseases. A thorough understanding of podocyte autophagy could shed novel insights into podocyte survival mechanisms with injury and offer potential targets for novel therapeutics for glomerular disease.
    Language English
    Publishing date 2021-03-12
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2662592-1
    ISSN 2077-0383
    ISSN 2077-0383
    DOI 10.3390/jcm10061184
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  8. Article ; Online: Recycling to discover something new: the role of autophagy in kidney disease.

    Leventhal, Jeremy S / Wyatt, Christina M / Ross, Michael J

    Kidney international

    2017  Volume 91, Issue 1, Page(s) 4–6

    Abstract: This year, the Nobel Prize in Physiology or Medicine was awarded to Yoshinori Ohsumi for his groundbreaking work in dissecting the mechanisms of autophagy, a cellular process resulting in the organized degradation of cytoplasmic components. Ohsumi's work ...

    Abstract This year, the Nobel Prize in Physiology or Medicine was awarded to Yoshinori Ohsumi for his groundbreaking work in dissecting the mechanisms of autophagy, a cellular process resulting in the organized degradation of cytoplasmic components. Ohsumi's work paved the way for subsequent studies that demonstrated critical roles for autophagy in modulating both acute and chronic kidney injury. This work may lead to future therapeutic approaches that target the autophagy system to prevent or treat kidney diseases.
    MeSH term(s) Autophagy/drug effects ; Autophagy/genetics ; Autophagy/physiology ; Humans ; Kidney/pathology ; Nobel Prize ; Physiology ; Renal Insufficiency, Chronic/pathology ; Renal Insufficiency, Chronic/physiopathology
    Language English
    Publishing date 2017-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2016.11.004
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    Zs.A 797: Show issues Location:
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  9. Article ; Online: Toll-like receptors in transplantation: sensing and reacting to injury.

    Leventhal, Jeremy S / Schröppel, Bernd

    Kidney international

    2012  Volume 81, Issue 9, Page(s) 826–832

    Abstract: Toll-like receptors (TLRs) are a family of transmembrane proteins that have a major role in pathogen-induced inflammation and orchestrating an organism's defense against infection. Data are emerging that the TLRs play an important role as a first ... ...

    Abstract Toll-like receptors (TLRs) are a family of transmembrane proteins that have a major role in pathogen-induced inflammation and orchestrating an organism's defense against infection. Data are emerging that the TLRs play an important role as a first response to tissue injury linking the innate with the adaptive immune system. The recognition that TLRs are expressed on nonimmune cells including renal and liver cells, and that endogenous, cell-derived ligands (damage-associated molecular patterns) can signal through specific TLRs has expanded the understanding of how these receptors impact a variety of diseases. This review focuses on recent findings elucidating the ability of TLRs to affect transplant outcomes. Specifically, observations demonstrating the link between endogenous TLR ligands and IR injury, how this can affect alloimmunity and transplant tolerance, and therapeutic implications will be discussed.
    MeSH term(s) Adaptive Immunity ; Animals ; Graft Rejection/immunology ; Graft Survival ; Humans ; Immunity, Innate ; Ligands ; Organ Transplantation/adverse effects ; Reperfusion Injury/immunology ; Signal Transduction ; Toll-Like Receptors/metabolism ; Transplantation Tolerance ; Treatment Outcome
    Chemical Substances Ligands ; Toll-Like Receptors
    Language English
    Publishing date 2012-02-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1038/ki.2011.498
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  10. Article ; Online: The diabetic microenvironment causes mitochondrial oxidative stress in glomerular endothelial cells and pathological crosstalk with podocytes.

    Casalena, Gabriella A / Yu, Liping / Gil, Roberto / Rodriguez, Samuel / Sosa, Shantel / Janssen, William / Azeloglu, Evren U / Leventhal, Jeremy S / Daehn, Ilse S

    Cell communication and signaling : CCS

    2020  Volume 18, Issue 1, Page(s) 105

    Abstract: Background: In the setting of diabetes mellitus, mitochondrial dysfunction and oxidative stress are important pathogenic mechanisms causing end organ damage, including diabetic kidney disease (DKD), but mechanistic understanding at a cellular level ... ...

    Abstract Background: In the setting of diabetes mellitus, mitochondrial dysfunction and oxidative stress are important pathogenic mechanisms causing end organ damage, including diabetic kidney disease (DKD), but mechanistic understanding at a cellular level remains obscure. In mouse models of DKD, glomerular endothelial cell (GEC) dysfunction precedes albuminuria and contributes to neighboring podocyte dysfunction, implicating GECs in breakdown of the glomerular filtration barrier. In the following studies we wished to explore the cellular mechanisms by which GECs become dysfunctional in the diabetic milieu, and the impact to neighboring podocytes.
    Methods: Mouse GECs were exposed to high glucose media (HG) or 2.5% v/v serum from diabetic mice or serum from non-diabetic controls, and evaluated for mitochondrial function (oxygen consumption), structure (electron microscopy), morphology (mitotracker), mitochondrial superoxide (mitoSOX), as well as accumulation of oxidized products (DNA lesion frequency (8-oxoG, endo-G), double strand breaks (γ-H2AX), endothelial function (NOS activity), autophagy (LC3) and apoptotic cell death (Annexin/PI; caspase 3). Supernatant transfer experiments from GECs to podocytes were performed to establish the effects on podocyte survival and transwell experiments were performed to determine the effects in co-culture.
    Results: Diabetic serum specifically causes mitochondrial dysfunction and mitochondrial superoxide release in GECs. There is a rapid oxidation of mitochondrial DNA and loss of mitochondrial biogenesis without cell death. Many of these effects are blocked by mitoTEMPO a selective mitochondrial anti-oxidant. Secreted factors from dysfunctional GECs were sufficient to cause podocyte apoptosis in supernatant transfer experiments, or in co-culture but this did not occur when GECs had been previously treated with mitoTEMPO.
    Conclusion: Dissecting the impact of the diabetic environment on individual cell-types from the kidney glomerulus indicates that GECs become dysfunctional and pathological to neighboring podocytes by increased levels of mitochondrial superoxide in GEC. These studies indicate that GEC-signaling to podocytes contributes to the loss of the glomerular filtration barrier in DKD. Video abstract.
    MeSH term(s) Animals ; Apoptosis ; Autophagy ; Cellular Microenvironment ; DNA, Mitochondrial/genetics ; Diabetes Mellitus, Experimental/pathology ; Endodeoxyribonucleases/metabolism ; Endothelial Cells/pathology ; Endothelial Cells/ultrastructure ; Kidney Glomerulus/pathology ; Male ; Mice ; Mitochondria/pathology ; Mitochondria/ultrastructure ; Mitochondrial Membranes/metabolism ; Mitochondrial Membranes/ultrastructure ; Oxidative Stress ; Podocytes/pathology ; Podocytes/ultrastructure
    Chemical Substances DNA, Mitochondrial ; Endodeoxyribonucleases (EC 3.1.-) ; endonuclease G (EC 3.1.21.-)
    Language English
    Publishing date 2020-07-08
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1478-811X
    ISSN (online) 1478-811X
    DOI 10.1186/s12964-020-00605-x
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