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Article: Recent Advances in the Roles of Autophagy and Autophagy Proteins in Host Cells During

Subauste, Carlos S

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 673813

Abstract: Toxoplasma ... ...

Abstract	Toxoplasma gondii
Language	English
Publishing date	2021-06-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.673813
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Article ; Online: The CD40-ATP-P2X

Subauste, Carlos S

Frontiers in immunology

2019 Volume 10, Page(s) 2958

Abstract: Extracellular adenosine 5'-triphosphate (ATP) functions not only as a neurotransmitter but is also released by non-excitable cells and mediates cell-cell communication involving glia. In pathological conditions, extracellular ATP released by astrocytes ... ...

Abstract	Extracellular adenosine 5'-triphosphate (ATP) functions not only as a neurotransmitter but is also released by non-excitable cells and mediates cell-cell communication involving glia. In pathological conditions, extracellular ATP released by astrocytes may act as a "danger" signal that activates microglia and promotes neuroinflammation. This review summarizes
MeSH term(s)	Adenosine Triphosphate/immunology ; Animals ; Apoptosis/immunology ; CD40 Antigens/immunology ; Capillaries/immunology ; Capillaries/pathology ; Cell Communication/immunology ; Endothelial Cells/immunology ; Endothelial Cells/pathology ; Humans ; Inflammation/immunology ; Inflammation/pathology ; Ischemia/immunology ; Ischemia/pathology ; Macrophages/immunology ; Macrophages/pathology ; Microglia/immunology ; Microglia/pathology ; Receptors, Purinergic P2X7/immunology ; Retinal Diseases/immunology ; Retinal Diseases/pathology ; Retinal Vessels/immunology ; Retinal Vessels/pathology
Chemical Substances	CD40 Antigens ; P2RX7 protein, human ; Receptors, Purinergic P2X7 ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2019-12-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.02958
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Article ; Online: Interplay Between

Subauste, Carlos S

Frontiers in cellular and infection microbiology

2019 Volume 9, Page(s) 139

Abstract: ... Survival ... ...

Abstract	Survival of
MeSH term(s)	Autophagy ; Host-Pathogen Interactions ; Immune Evasion ; Toxoplasma/growth & development ; Toxoplasma/immunology ; Toxoplasmosis/immunology ; Toxoplasmosis/parasitology
Language	English
Publishing date	2019-05-01
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2019.00139
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Article ; Online: Advanced Glycation End Products Upregulate CD40 in Human Retinal Endothelial and Müller Cells: Relevance to Diabetic Retinopathy.

Portillo, Jose-Andres C / Pfaff, Amelia / Vos, Sarah / Weng, Matthew / Nagaraj, Ram H / Subauste, Carlos S

Cells

2024 Volume 13, Issue 5

Abstract: CD40 induces pro-inflammatory responses in endothelial and Müller cells and is required for the development of diabetic retinopathy (DR). CD40 is upregulated in these cells in patients with DR. CD40 upregulation is a central feature of CD40-driven ... ...

Abstract	CD40 induces pro-inflammatory responses in endothelial and Müller cells and is required for the development of diabetic retinopathy (DR). CD40 is upregulated in these cells in patients with DR. CD40 upregulation is a central feature of CD40-driven inflammatory disorders. What drives CD40 upregulation in the diabetic retina remains unknown. We examined the role of advanced glycation end products (AGEs) in CD40 upregulation in endothelial cells and Müller cells. Human endothelial cells and Müller cells were incubated with unmodified or methylglyoxal (MGO)-modified fibronectin. CD40 expression was assessed by flow cytometry. The expression of ICAM-1 and CCL2 was examined by flow cytometry or ELISA after stimulation with CD154 (CD40 ligand). The expression of carboxymethyl lysine (CML), fibronectin, and laminin as well as CD40 in endothelial and Müller cells from patients with DR was examined by confocal microscopy. Fibronectin modified by MGO upregulated CD40 in endothelial and Müller cells. CD40 upregulation was functionally relevant. MGO-modified fibronectin enhanced CD154-driven upregulation of ICAM-1 and CCL2 in endothelial and Müller cells. Increased CD40 expression in endothelial and Müller cells from patients with DR was associated with increased CML expression in fibronectin and laminin. These findings identify AGEs as inducers of CD40 upregulation in endothelial and Müller cells and enhancers of CD40-dependent pro-inflammatory responses. CD40 upregulation in these cells is associated with higher CML expression in fibronectin and laminin in patients with DR. This study revealed that CD40 and AGEs, two important drivers of DR, are interconnected.
MeSH term(s)	Humans ; Diabetic Retinopathy/metabolism ; Intercellular Adhesion Molecule-1/metabolism ; Fibronectins/metabolism ; Ependymoglial Cells/metabolism ; Endothelial Cells/metabolism ; Magnesium Oxide/metabolism ; Retina/metabolism ; CD40 Antigens/metabolism ; CD40 Ligand/metabolism ; Laminin/metabolism ; Glycation End Products, Advanced/metabolism ; Diabetes Mellitus/metabolism
Chemical Substances	Intercellular Adhesion Molecule-1 (126547-89-5) ; Fibronectins ; Magnesium Oxide (3A3U0GI71G) ; CD40 Antigens ; CD40 Ligand (147205-72-9) ; Laminin ; Glycation End Products, Advanced
Language	English
Publishing date	2024-02-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells13050429
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Article ; Online: CD40, a Novel Inducer of Purinergic Signaling: Implications to the Pathogenesis of Experimental Diabetic Retinopathy.

Subauste, Carlos S

Vision (Basel, Switzerland)

2017 Volume 1, Issue 3

Abstract: Diabetic retinopathy is a leading complication of diabetes. Death of capillary cells with resulting capillary degeneration is a central feature of this disease. Chronic low-grade inflammation has been linked to the development of retinal capillary ... ...

Abstract	Diabetic retinopathy is a leading complication of diabetes. Death of capillary cells with resulting capillary degeneration is a central feature of this disease. Chronic low-grade inflammation has been linked to the development of retinal capillary degeneration in diabetes. CD40 is an upstream inducer of a broad range of inflammatory responses in the diabetic retina and is required for death of retinal capillary cells. Recent studies uncovered CD40 as a novel inducer of purinergic signaling and identified the CD40-ATP-P2X
Language	English
Publishing date	2017-08-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ISSN	2411-5150
ISSN (online)	2411-5150
DOI	10.3390/vision1030020
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Article ; Online: CD40 Upregulation in the Retina of Patients With Diabetic Retinopathy: Association With TRAF2/TRAF6 Upregulation and Inflammatory Molecule Expression.

Vos, Sarah / Aaron, Rachel / Weng, Matthew / Daw, Jad / Rodriguez-Rivera, Emmanuel / Subauste, Carlos S

Investigative ophthalmology & visual science

2023 Volume 64, Issue 7, Page(s) 17

Abstract: Purpose: CD40 is upregulated in the retinas of diabetic mice, drives pro-inflammatory molecule expression, and promotes diabetic retinopathy. The role of CD40 in diabetic retinopathy in humans is unknown. Upregulation of CD40 and its downstream ... ...

Abstract	Purpose: CD40 is upregulated in the retinas of diabetic mice, drives pro-inflammatory molecule expression, and promotes diabetic retinopathy. The role of CD40 in diabetic retinopathy in humans is unknown. Upregulation of CD40 and its downstream signaling molecules TNF receptor associated factors (TRAFs) is a key feature of CD40-driven inflammatory disorders. We examined the expression of CD40, TRAF2, and TRAF6 as well as pro-inflammatory molecules in retinas from patients with diabetic retinopathy. Methods: Posterior poles from patients with diabetic retinopathy and non-diabetic controls were stained with antibodies against von Willebrand factor (labels endothelial cells), cellular retinaldehyde-binding protein (CRALBP), or vimentin (both label Müller cells) plus antibodies against CD40, TRAF2, TRAF6, ICAM-1, CCL2, TNF-α, and/or phospho-Tyr783 phospholipase Cγ1 (PLCγ1). Sections were analyzed by confocal microscopy. Results: CD40 expression was increased in endothelial and Müller cells from patients with diabetic retinopathy. CD40 was co-expressed with ICAM-1 in endothelial cells and with CCL2 in Müller cells. TNF-α was detected in retinal cells from these patients, but these cells lacked endothelial/Müller cell markers. CD40 in Müller cells from patients with diabetic retinopathy co-expressed activated phospholipase Cγ1, a molecule that induces TNF-α expression in myeloid cells in mice. CD40 upregulation in endothelial cells and Müller cells from patients with diabetic retinopathy was accompanied by TRAF2 and TRAF6 upregulation. Conclusions: CD40, TRAF2, and TRAF6 are upregulated in patients with diabetic retinopathy. CD40 associates with expression of pro-inflammatory molecules. These findings suggest that CD40-TRAF signaling may promote pro-inflammatory responses in the retinas of patients with diabetic retinopathy.
MeSH term(s)	Humans ; Mice ; Animals ; TNF Receptor-Associated Factor 2/genetics ; TNF Receptor-Associated Factor 2/metabolism ; Diabetic Retinopathy/metabolism ; TNF Receptor-Associated Factor 6/metabolism ; Intercellular Adhesion Molecule-1/metabolism ; Up-Regulation ; Endothelial Cells/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Diabetes Mellitus, Experimental/metabolism ; CD40 Antigens/genetics ; Retina/metabolism ; Phospholipases/metabolism
Chemical Substances	TNF Receptor-Associated Factor 2 ; TNF Receptor-Associated Factor 6 ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Tumor Necrosis Factor-alpha ; CD40 Antigens ; Phospholipases (EC 3.1.-)
Language	English
Publishing date	2023-04-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.64.7.17
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Article ; Online: CD40 Expressed in Endothelial Cells Promotes Upregulation of ICAM-1 But Not Pro-Inflammatory Cytokines, NOS2 and P2X7 in the Diabetic Retina.

Yu, Jin-Sang / Daw, Jad / Portillo, Jose-Andres C / Subauste, Carlos S

Investigative ophthalmology & visual science

2021 Volume 62, Issue 12, Page(s) 22

Abstract: Purpose: CD40 is an upstream inducer of inflammation in the diabetic retina. CD40 is upregulated in retinal endothelial cells in diabetes. The purpose of this study was to determine whether expression of CD40 in endothelial cells is sufficient to ... ...

Abstract	Purpose: CD40 is an upstream inducer of inflammation in the diabetic retina. CD40 is upregulated in retinal endothelial cells in diabetes. The purpose of this study was to determine whether expression of CD40 in endothelial cells is sufficient to promote inflammatory responses in the retina of diabetic mice. Methods: Transgenic mice with CD40 expression restricted to endothelial cells (Trg-CD40 EC), transgenic control mice (Trg-Ctr), B6, and CD40-/- mice were made diabetic using streptozotocin. Leukostasis was assessed using FITC-conjugated ConA. Pro-inflammatory molecule expression was examined by real-time PCR, immunohistochemistry, ELISA, or flow cytometry. Release of ATP was assessed by ATP bioluminescence. Results: Diabetic B6 and Trg-CD40 EC mice exhibited increased retinal mRNA levels of ICAM-1, higher ICAM-1 expression in endothelial cells, and increased leukostasis. These responses were not detected in diabetic mice that lacked CD40 (CD40-/- and Trg-Ctr). Diabetic B6 but not Trg-CD40 EC mice upregulated TNF-α, IL-1β, and NOS2 mRNA levels. CD40 stimulation in retinal endothelial cells upregulated ICAM-1 but not TNF-α, IL-1β, or NOS2. CD40 ligation did not trigger ATP release by retinal endothelial cells or pro-inflammatory cytokine production in bystander myeloid cells. In contrast to diabetic B6 mice, diabetic Trg-CD40 EC mice did not upregulate P2X7 mRNA levels in the retina. Conclusions: Endothelial cell CD40 promotes ICAM-1 upregulation and leukostasis. In contrast, endothelial cell CD40 does not lead to pro-inflammatory cytokine and NOS2 upregulation likely because it does not activate purinergic-mediated pro-inflammatory molecule expression by myeloid cells or induce expression of these pro-inflammatory molecules in endothelial cells.
MeSH term(s)	Animals ; CD40 Antigens/genetics ; Cytokines/genetics ; Diabetes Mellitus, Experimental/genetics ; Diabetic Retinopathy/genetics ; Endothelial Cells/metabolism ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Gene Expression Regulation/physiology ; Humans ; Intercellular Adhesion Molecule-1/genetics ; Leukostasis ; Luminescent Measurements ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nitric Oxide Synthase Type II/genetics ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Receptors, Purinergic P2X7/genetics ; Retinal Vessels/cytology ; Up-Regulation
Chemical Substances	CD40 Antigens ; Cytokines ; Icam1 protein, mouse ; P2rx7 protein, mouse ; RNA, Messenger ; Receptors, Purinergic P2X7 ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, mouse (EC 1.14.13.39)
Language	English
Publishing date	2021-09-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.62.12.22
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Article ; Online: Epidermal growth factor receptor promotes cerebral and retinal invasion by Toxoplasma gondii.

Corcino, Yalitza Lopez / Portillo, Jose-Andres C / Subauste, Carlos S

Scientific reports

2019 Volume 9, Issue 1, Page(s) 669

Abstract: Little is known about strategies used by pathogens to facilitate CNS invasion. Toxoplasma gondii reaches the CNS by circulating in blood within leukocytes or as extracellular tachyzoites. T. gondii induces EGFR signaling in vitro during invasion of ... ...

Abstract	Little is known about strategies used by pathogens to facilitate CNS invasion. Toxoplasma gondii reaches the CNS by circulating in blood within leukocytes or as extracellular tachyzoites. T. gondii induces EGFR signaling in vitro during invasion of mammalian cells. We examined the effects of endothelial cell EGFR on CNS invasion. Transgenic mice whose endothelial cells expressed a dominant negative (DN) EGFR (inhibits EGFR signaling) exhibited diminished parasite load and histopathology in the brain and retina after T. gondii infection. I.V. administration of infected leukocytes or extracellular tachyzoites led to reduced parasite loads in mice with DN EGFR. This was not explained by enhanced immunity or reduced leukocyte recruitment. Endothelial cell infection is key for CNS invasion. Parasite foci in brain endothelial cells were reduced by DN EGFR. DN EGFR in these cells led to recruitment of the autophagy protein LC3 around T. gondii and spontaneous parasite killing dependent on the autophagy protein ULK1 and lysosomal enzymes. The autophagy inhibitor 3-MA prevented DN EGFR mice from exhibiting reduced CNS invasion. Altogether, EGFR is a novel regulator of T. gondii invasion of neural tissue, enhancing invasion likely by promoting survival of the parasite within endothelial cells.
MeSH term(s)	Animals ; Autophagy ; Brain/parasitology ; Brain/pathology ; Endothelial Cells/metabolism ; Endothelial Cells/parasitology ; ErbB Receptors/genetics ; ErbB Receptors/metabolism ; Female ; Host-Parasite Interactions/physiology ; Immunity, Humoral ; Leukocytes/pathology ; Mice, Transgenic ; Parasite Load ; Retina/parasitology ; Retina/pathology ; Toxoplasma/pathogenicity ; Toxoplasmosis/immunology ; Toxoplasmosis/metabolism ; Toxoplasmosis/parasitology
Chemical Substances	EGFR protein, mouse (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2019-01-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-36724-2
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Article: Autophagy in immunity against Toxoplasma gondii.

Subauste, Carlos S

Current topics in microbiology and immunology

2009 Volume 335, Page(s) 251–265

Abstract: A decisive outcome during host-pathogen interaction is governed by whether pathogen-containing vacuoles fuse with lysosomes. Fusion with lysosomes typically kills microbes. Toxoplasma gondii represents a classical example of an intracellular pathogen ... ...

Abstract	A decisive outcome during host-pathogen interaction is governed by whether pathogen-containing vacuoles fuse with lysosomes. Fusion with lysosomes typically kills microbes. Toxoplasma gondii represents a classical example of an intracellular pathogen that survives within host cells by preventing the endosomal-lysosomal compartments from fusing with the vacuoles that contain the pathogen. Thus, T. gondii provides an excellent model to determine if the immune system can target a pathogen for lysosomal degradation. CD40, a major regulator of cell-mediated immunity, activates macrophages to kill T. gondii through a process that requires recruitment of autophagosomes around the parasitophorous vacuole, leading to lysosomal degradation of the parasite. These studies demonstrate that cell-mediated immunity can activate autophagy to kill a pathogen. CD40-induced autophagy likely contributes to resistance against T. gondii, particularly in neural tissues, the main sites affected by this pathogen.
MeSH term(s)	Animals ; Autophagy/immunology ; CD40 Antigens/immunology ; Humans ; Lysosomes/immunology ; Lysosomes/parasitology ; Toxoplasma/immunology ; Toxoplasmosis/immunology ; Vacuoles/immunology ; Vacuoles/parasitology
Chemical Substances	CD40 Antigens
Language	English
Publishing date	2009-09-04
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	0070-217X
ISSN	0070-217X
DOI	10.1007/978-3-642-00302-8_12
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Article ; Online: CD40 and the immune response to parasitic infections.

Subauste, Carlos S

Seminars in immunology

2009 Volume 21, Issue 5, Page(s) 273–282

Abstract: The interaction between CD40 and CD154 regulates many aspects of cellular and humoral immunity. The CD40-CD154 pathway is important for resistance against a variety of parasites. Studies done with these pathogens have provided important insight into the ... ...

Abstract	The interaction between CD40 and CD154 regulates many aspects of cellular and humoral immunity. The CD40-CD154 pathway is important for resistance against a variety of parasites. Studies done with these pathogens have provided important insight into the various mechanisms by which this pathway enhances host protection, mechanisms by which pathogens subvert CD40 signaling, conditions in which the CD40-CD154 pathway promotes disease and on modulation of this pathway for immunotherapy.
MeSH term(s)	Animals ; CD40 Antigens/immunology ; CD40 Ligand/immunology ; Humans ; Parasitic Diseases/immunology ; Signal Transduction/immunology
Chemical Substances	CD40 Antigens ; CD40 Ligand (147205-72-9)
Language	English
Publishing date	2009-07-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1018141-6
ISSN	1096-3618 ; 1044-5323
ISSN (online)	1096-3618
ISSN	1044-5323
DOI	10.1016/j.smim.2009.06.003
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