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Article ; Online: P2X7-dependent immune pathways in retinal diseases.

Déchelle-Marquet, Paul-Alexandre / Guillonneau, Xavier / Sennlaub, Florian / Delarasse, Cécile

2022 Volume 223, Page(s) 109332

Abstract: Adenosine triphosphate (ATP) is a signalling molecule acting as a neurotransmitter but also as a danger signal. The purinergic receptor P2X7 is the main sensor of high concentration of ATP released by damaged cells. In the eye, P2X7 is expressed by ... ...

Abstract	Adenosine triphosphate (ATP) is a signalling molecule acting as a neurotransmitter but also as a danger signal. The purinergic receptor P2X7 is the main sensor of high concentration of ATP released by damaged cells. In the eye, P2X7 is expressed by resident microglia and immune cells that infiltrate the retina in disease such as age-related macular degeneration (AMD), a degenerative retinal disease, and uveitis, an inflammatory eye disease. Activation of P2X7 is involved in several physiological and pathological processes: phagocytosis, activation of the inflammasome NLRP3, release of pro-inflammatory mediators and cell death. The aim of this review is to discuss the potential involvement of P2X7 in the development of AMD and uveitis.
Language	English
Publishing date	2022-11-11
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2022.109332
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Article: Pleiotropic Roles of P2X7 in the Central Nervous System.

Kanellopoulos, Jean M / Delarasse, Cécile

Frontiers in cellular neuroscience

2019 Volume 13, Page(s) 401

Abstract: The purinergic receptor P2X7 is expressed in neural and immune cells known to be involved in neurological diseases. Its ligand, ATP, is a signaling molecule that can act as a neurotransmitter in physiological conditions or as a danger signal when ... ...

Abstract	The purinergic receptor P2X7 is expressed in neural and immune cells known to be involved in neurological diseases. Its ligand, ATP, is a signaling molecule that can act as a neurotransmitter in physiological conditions or as a danger signal when released in high amount by damaged/dying cells or activated glial cells. Thus, ATP is a danger-associated molecular pattern. Binding of ATP by P2X7 leads to the activation of different biochemical pathways, depending on the physiological or pathological environment. The aim of this review is to discuss various functions of P2X7 in the immune and central nervous systems. We present evidence that P2X7 may have a detrimental or beneficial role in the nervous system, in the context of neurological pathologies: epilepsy, Alzheimer's disease, multiple sclerosis, amyotrophic lateral sclerosis, age-related macular degeneration and cerebral artery occlusion.
Language	English
Publishing date	2019-09-04
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2019.00401
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Article ; Online: The P2X7 Receptor, a Multifaceted Receptor in Alzheimer's Disease.

Ronning, Kaitryn E / Déchelle-Marquet, Paul-Alexandre / Che, Yueshen / Guillonneau, Xavier / Sennlaub, Florian / Delarasse, Cécile

International journal of molecular sciences

2023 Volume 24, Issue 14

Abstract: Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by impaired episodic memory and two pathological lesions: amyloid plaques and neurofibrillary tangles. In AD, damaged neurons and the accumulation of amyloid β (Aβ) ... ...

Abstract	Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by impaired episodic memory and two pathological lesions: amyloid plaques and neurofibrillary tangles. In AD, damaged neurons and the accumulation of amyloid β (Aβ) peptides cause a significant release of high amounts of extracellular ATP, which acts as a danger signal. The purinergic receptor P2X7 is the main sensor of high concentrations of ATP, and P2X7 has been shown to be upregulated in the brains of AD patients, contributing to the disease's pathological processes. Further, there are many polymorphisms of the
MeSH term(s)	Humans ; Adenosine Triphosphate/metabolism ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/genetics ; Amyloid beta-Peptides/metabolism ; Microglia/metabolism ; Neurodegenerative Diseases/metabolism ; Receptors, Purinergic P2X7/genetics ; Receptors, Purinergic P2X7/metabolism
Chemical Substances	Adenosine Triphosphate (8L70Q75FXE) ; Amyloid beta-Peptides ; Receptors, Purinergic P2X7 ; P2RX7 protein, human
Language	English
Publishing date	2023-07-21
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241411747
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Article ; Online: Complex role of chemokine mediators in animal models of Alzheimer's Disease.

Martin, Elodie / Delarasse, Cécile

Biomedical journal

2018 Volume 41, Issue 1, Page(s) 34–40

Abstract: Chemokines are a family of cytokines, first described to play a role in the immune system. However, neurons and glial cells also express chemokines and their receptors. In the central nervous system, chemokines are involved in several neural functions, ... ...

Abstract	Chemokines are a family of cytokines, first described to play a role in the immune system. However, neurons and glial cells also express chemokines and their receptors. In the central nervous system, chemokines are involved in several neural functions, in particular in the control of cell communications and neuronal activity. In pathological conditions, chemokines participate in neuroinflammatory and neurodegenerative processes. In Alzheimer's disease (AD), chemokines play a role in the development of the two main lesions, amyloid β plaques and neurofibrillary tangles. In addition, they contribute to the inflammatory response by recruiting T cells and controlling microglia/macrophages activation. Actually, targeting inflammatory pathways seems a promising therapeutic approach for the treatment of AD patients. This review summarizes our current knowledge on the roles of chemokines in AD animal models and the underlying mechanisms in which they take part. Better knowledge of the role of chemokines and their cellular receptors in AD could open new therapeutic perspectives.
MeSH term(s)	Alzheimer Disease/etiology ; Animals ; Chemokines/physiology ; Disease Models, Animal ; Humans ; Inflammation/etiology
Chemical Substances	Chemokines
Language	English
Publishing date	2018-03-27
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2698541-X
ISSN	2320-2890 ; 2319-4170
ISSN (online)	2320-2890
ISSN	2319-4170
DOI	10.1016/j.bj.2018.01.002
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Article ; Online: Le récepteur P2X7, une nouvelle cible thérapeutique dans la maladie d’Alzheimer.

Martin, Elodie / Kanellopoulos, Jean / Fontaine, Bertrand / Delatour, Benoît / Delarasse, Cécile

Medecine sciences : M/S

2019 Volume 35, Issue 2, Page(s) 97–99

Title translation	The purinergic receptor P2X7, a new therapeutic target in Alzheimer' disease.
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/therapy ; Animals ; Disease Models, Animal ; Humans ; Mice ; Mice, Transgenic ; Molecular Targeted Therapy/methods ; Molecular Targeted Therapy/trends ; Receptors, Purinergic P2X7/physiology ; Therapies, Investigational
Chemical Substances	Receptors, Purinergic P2X7
Language	French
Publishing date	2019-02-18
Publishing country	France
Document type	News
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/2019017
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Article ; Online: Sur les origines inflammatoires de la DMLA.

Roubeix, Christophe / Sahel, José-Alain / Guillonneau, Xavier / Delarasse, Cécile / Sennlaub, Florian

Medecine sciences : M/S

2020 Volume 36, Issue 10, Page(s) 886–892

Abstract: Age-related macular degeneration (AMD) is a complex, highly heritable, multifactorial disease caused by the interplay of age and genetic and environmental risk factors. No treatment has yet been found to treat the slowly progressing atrophic form of AMD. ...

Title translation	On the inflammatory origins of AMD.
Abstract	Age-related macular degeneration (AMD) is a complex, highly heritable, multifactorial disease caused by the interplay of age and genetic and environmental risk factors. No treatment has yet been found to treat the slowly progressing atrophic form of AMD. All forms of AMD are invariably associated with an accumulation of mononuclear phagocytes (MP) in the subretinal space, a family of cells that include inflammatory and resident macrophages. We here present an overview of the inflammatory process occurring in AMD and discuss the origin of MPs and the consequences of their accumulation in the subretinal space. Finally, we will review the role played by the established risk factors for AMD to promote the switch from beneficial inflammation in early stage to a deleterious inflammation in the advanced stage of the disease.
MeSH term(s)	Eye/immunology ; Eye/metabolism ; Eye/pathology ; Humans ; Immune Privilege/physiology ; Inflammation/complications ; Inflammation/metabolism ; Inflammation Mediators/metabolism ; Inflammation Mediators/physiology ; Macular Degeneration/epidemiology ; Macular Degeneration/etiology ; Macular Degeneration/immunology ; Macular Degeneration/metabolism ; Risk Factors
Chemical Substances	Inflammation Mediators
Language	French
Publishing date	2020-10-07
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/2020159
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Article ; Online: Distinct inflammatory phenotypes of microglia and monocyte-derived macrophages in Alzheimer's disease models: effects of aging and amyloid pathology.

Martin, Elodie / Boucher, Céline / Fontaine, Bertrand / Delarasse, Cécile

Aging cell

2017 Volume 16, Issue 1, Page(s) 27–38

Abstract: Alzheimer's disease (AD) is a neurodegenerative disease characterized by formation of amyloid-β (Aβ) plaques, activated microglia, and neuronal cell death leading to progressive dementia. Recent data indicate that microglia and monocyte-derived ... ...

Abstract	Alzheimer's disease (AD) is a neurodegenerative disease characterized by formation of amyloid-β (Aβ) plaques, activated microglia, and neuronal cell death leading to progressive dementia. Recent data indicate that microglia and monocyte-derived macrophages (MDM) are key players in the initiation and progression of AD, yet their respective roles remain to be clarified. As AD occurs mostly in the elderly and aging impairs myeloid functions, we addressed the inflammatory profile of microglia and MDM during aging in TgAPP/PS1 and TgAPP/PS1dE9, two transgenic AD mouse models, compared to WT littermates. We only found MDM infiltration in very aged mice. We determined that MDM highly expressed activation markers at basal state. In contrast, microglia exhibited an activated phenotype only with normal aging and Aβ pathology. Our study showed that CD14 and CD36, two receptors involved in phagocytosis, were upregulated during Aβ pathogenesis. Moreover, we observed, at the protein levels in AD models, higher production of pro-inflammatory mediators: IL-1β, p40, iNOS, CCL-3, CCL-4, and CXCL-1. Taken together, our data indicate that microglia and MDM display distinct phenotypes in AD models and highlight the specific effects of normal aging vs Aβ peptides on inflammatory processes that occur during the disease progression. These precise phenotypes of different subpopulations of myeloid cells in normal and pathologic conditions may allow the design of pertinent therapeutic strategy for AD.
MeSH term(s)	Aging/pathology ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Animals ; CD36 Antigens/metabolism ; Chemokines/metabolism ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Inflammation/pathology ; Lipopolysaccharide Receptors/metabolism ; Macrophages/pathology ; Mice, Inbred C57BL ; Mice, Transgenic ; Microglia/pathology ; Models, Biological ; Monocytes/pathology ; Myeloid Cells/metabolism ; Nitric Oxide Synthase Type II/metabolism ; Phagocytosis ; Phenotype ; Plaque, Amyloid/pathology
Chemical Substances	Amyloid beta-Peptides ; CD36 Antigens ; Chemokines ; Lipopolysaccharide Receptors ; Nitric Oxide Synthase Type II (EC 1.14.13.39)
Language	English
Publishing date	2017-02
Publishing country	England
Document type	Journal Article
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.12522
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Article ; Online: Splenic monocytes drive pathogenic subretinal inflammation in age-related macular degeneration.

Roubeix, Christophe / Nous, Caroline / Augustin, Sébastien / Ronning, Kaitryn E / Mathis, Thibaud / Blond, Frédéric / Lagouge-Roussey, Pauline / Crespo-Garcia, Sergio / Sullivan, Patrick M / Gautier, Emmanuel L / Reichhart, Nadine / Sahel, José-Alain / Burns, Marie E / Paques, Michel / Sørensen, Torben Lykke / Strauss, Olaf / Guillonneau, Xavier / Delarasse, Cécile / Sennlaub, Florian

Journal of neuroinflammation

2024 Volume 21, Issue 1, Page(s) 22

Abstract: Age-related macular degeneration (AMD) is invariably associated with the chronic accumulation of activated mononuclear phagocytes in the subretinal space. The mononuclear phagocytes are composed of microglial cells but also of monocyte-derived cells, ... ...

Abstract	Age-related macular degeneration (AMD) is invariably associated with the chronic accumulation of activated mononuclear phagocytes in the subretinal space. The mononuclear phagocytes are composed of microglial cells but also of monocyte-derived cells, which promote photoreceptor degeneration and choroidal neovascularization. Infiltrating blood monocytes can originate directly from bone marrow, but also from a splenic reservoir, where bone marrow monocytes develop into angiotensin II receptor (ATR1)
MeSH term(s)	Humans ; Mice ; Animals ; Aged ; Monocytes/pathology ; Angiotensin II ; Macular Degeneration/genetics ; Inflammation/genetics ; Choroidal Neovascularization
Chemical Substances	Angiotensin II (11128-99-7)
Language	English
Publishing date	2024-01-17
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-024-03011-z
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Article ; Online: Melanophages give rise to hyperreflective foci in AMD, a disease-progression marker.

Augustin, Sebastien / Lam, Marion / Lavalette, Sophie / Verschueren, Anna / Blond, Frédéric / Forster, Valérie / Przegralek, Lauriane / He, Zhiguo / Lewandowski, Daniel / Bemelmans, Alexis-Pierre / Picaud, Serge / Sahel, José-Alain / Mathis, Thibaud / Paques, Michel / Thuret, Gilles / Guillonneau, Xavier / Delarasse, Cécile / Sennlaub, Florian

Journal of neuroinflammation

2023 Volume 20, Issue 1, Page(s) 28

Abstract: Retinal melanosome/melanolipofuscin-containing cells (MCCs), clinically visible as hyperreflective foci (HRF) and a highly predictive imaging biomarker for the progression of age-related macular degeneration (AMD), are widely believed to be migrating ... ...

Abstract	Retinal melanosome/melanolipofuscin-containing cells (MCCs), clinically visible as hyperreflective foci (HRF) and a highly predictive imaging biomarker for the progression of age-related macular degeneration (AMD), are widely believed to be migrating retinal pigment epithelial (RPE) cells. Using human donor tissue, we identify the vast majority of MCCs as melanophages, melanosome/melanolipofuscin-laden mononuclear phagocytes (MPs). Using serial block-face scanning electron microscopy, RPE flatmounts, bone marrow transplantation and in vitro experiments, we show how retinal melanophages form by the transfer of melanosomes from the RPE to subretinal MPs when the "don't eat me" signal CD47 is blocked. These melanophages give rise to hyperreflective foci in Cd47
MeSH term(s)	Humans ; Animals ; Mice ; CD47 Antigen/metabolism ; Retinal Pigment Epithelium/metabolism ; Macular Degeneration/metabolism ; Retina/metabolism ; Tomography, Optical Coherence/methods
Chemical Substances	CD47 Antigen
Language	English
Publishing date	2023-02-08
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-023-02699-9
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Article ; Online: Analysis of Microglia and Monocyte-derived Macrophages from the Central Nervous System by Flow Cytometry.

Martin, Elodie / El-Behi, Mohamed / Fontaine, Bertrand / Delarasse, Cecile

Journal of visualized experiments : JoVE

2017 , Issue 124

Abstract: Numerous studies have demonstrated the role of immune cells, in particular macrophages, in central nervous system (CNS) pathologies. There are two main macrophage populations in the CNS: (i) the microglia, which are the resident macrophages of the CNS ... ...

Abstract	Numerous studies have demonstrated the role of immune cells, in particular macrophages, in central nervous system (CNS) pathologies. There are two main macrophage populations in the CNS: (i) the microglia, which are the resident macrophages of the CNS and are derived from yolk sac progenitors during embryogenesis, and (ii) the monocyte-derived macrophages (MDM), which can infiltrate the CNS during disease and are derived from bone marrow progenitors. The roles of each macrophage subpopulation differ depending on the pathology being studied. Furthermore, there is no consensus on the histological markers or the distinguishing criteria used for these macrophage subpopulations. However, the analysis of the expression profiles of the CD11b and CD45 markers by flow cytometry allows us to distinguish the microglia (CD11b
MeSH term(s)	Animals ; Biomarkers/analysis ; CD11b Antigen/biosynthesis ; Central Nervous System/cytology ; Central Nervous System/immunology ; Flow Cytometry/methods ; Leukocyte Common Antigens/biosynthesis ; Macrophages/cytology ; Macrophages/immunology ; Mice ; Microglia/cytology ; Microglia/immunology
Chemical Substances	Biomarkers ; CD11b Antigen ; Leukocyte Common Antigens (EC 3.1.3.48) ; Ptprc protein, mouse (EC 3.1.3.48)
Language	English
Publishing date	2017-06-22
Publishing country	United States
Document type	Journal Article ; Video-Audio Media
ISSN	1940-087X
ISSN (online)	1940-087X
DOI	10.3791/55781
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