Microglia-derived CCL2 has a prime role in neocortex neuroinflammation
Background In myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), several areas of demyelination are detectable in mouse cerebral cortex, where neuroinflammation events are associated with scarce inflammatory infiltrates and blood–brain barrier (BBB) im...
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| Autor*in: |
Errede, Mariella [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022 |
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| Schlagwörter: |
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| Anmerkung: |
© The Author(s) 2022 |
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| Übergeordnetes Werk: |
Enthalten in: Cerebrospinal fluid research - London : BioMed Central, 2004, 19(2022), 1 vom: 30. Aug. |
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| Übergeordnetes Werk: |
volume:19 ; year:2022 ; number:1 ; day:30 ; month:08 |
| Links: |
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| DOI / URN: |
10.1186/s12987-022-00365-5 |
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SPR05095685X |
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| 520 | |a Background In myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), several areas of demyelination are detectable in mouse cerebral cortex, where neuroinflammation events are associated with scarce inflammatory infiltrates and blood–brain barrier (BBB) impairment. In this condition, the administration of mesenchymal stem cells (MSCs) controls neuroinflammation, attenuating astrogliosis and promoting the acquisition of stem cell traits by astrocytes. To contribute to the understanding of the mechanisms involved in the pathogenesis of EAE in gray matter and in the reverting effects of MSC treatment, the neocortex of EAE-affected mice was investigated by analyzing the cellular source(s) of chemokine CCL2, a molecule involved in immune cell recruitment and BBB-microvessel leakage. Methods The study was carried out by immunohistochemistry (IHC) and dual RNAscope IHC/in situ hybridization methods, using astrocyte, NG2-glia, macrophage/microglia, and microglia elective markers combined with CCL2. Results The results showed that in EAE-affected mice, hypertrophic microglia are the primary source of CCL2, surround the cortex neurons and the damaged BBB microvessels. In EAE-affected mice treated with MSCs, microgliosis appeared diminished very soon (6 h) after treatment, an observation that was long-lasting (tested after 10 days). This was associated with a reduced CCL2 expression and with apparently preserved/restored BBB features. In conclusion, the hallmark of EAE in the mouse neocortex is a condition of microgliosis characterized by high levels of CCL2 expression. Conclusions This finding supports relevant pathogenetic and clinical aspects of the human disease, while the demonstrated early control of neuroinflammation and BBB permeability exerted by treatment with MSCs may have important therapeutic implications. | ||
| 650 | 4 | |a Experimental autoimmune encephalomyelitis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Neocortex |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Microglia |7 (dpeaa)DE-He213 | |
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10.1186/s12987-022-00365-5 doi (DE-627)SPR05095685X (SPR)s12987-022-00365-5-e DE-627 ger DE-627 rakwb eng Errede, Mariella verfasserin aut Microglia-derived CCL2 has a prime role in neocortex neuroinflammation 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background In myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), several areas of demyelination are detectable in mouse cerebral cortex, where neuroinflammation events are associated with scarce inflammatory infiltrates and blood–brain barrier (BBB) impairment. In this condition, the administration of mesenchymal stem cells (MSCs) controls neuroinflammation, attenuating astrogliosis and promoting the acquisition of stem cell traits by astrocytes. To contribute to the understanding of the mechanisms involved in the pathogenesis of EAE in gray matter and in the reverting effects of MSC treatment, the neocortex of EAE-affected mice was investigated by analyzing the cellular source(s) of chemokine CCL2, a molecule involved in immune cell recruitment and BBB-microvessel leakage. Methods The study was carried out by immunohistochemistry (IHC) and dual RNAscope IHC/in situ hybridization methods, using astrocyte, NG2-glia, macrophage/microglia, and microglia elective markers combined with CCL2. Results The results showed that in EAE-affected mice, hypertrophic microglia are the primary source of CCL2, surround the cortex neurons and the damaged BBB microvessels. In EAE-affected mice treated with MSCs, microgliosis appeared diminished very soon (6 h) after treatment, an observation that was long-lasting (tested after 10 days). This was associated with a reduced CCL2 expression and with apparently preserved/restored BBB features. In conclusion, the hallmark of EAE in the mouse neocortex is a condition of microgliosis characterized by high levels of CCL2 expression. Conclusions This finding supports relevant pathogenetic and clinical aspects of the human disease, while the demonstrated early control of neuroinflammation and BBB permeability exerted by treatment with MSCs may have important therapeutic implications. Experimental autoimmune encephalomyelitis (dpeaa)DE-He213 Neocortex (dpeaa)DE-He213 Microglia (dpeaa)DE-He213 CCL2 (dpeaa)DE-He213 Mesenchymal stem cells (dpeaa)DE-He213 Annese, Tiziana aut Petrosino, Valentina aut Longo, Giovanna aut Girolamo, Francesco aut de Trizio, Ignazio aut d’Amati, Antonio aut Uccelli, Antonio aut Kerlero de Rosbo, Nicole aut Virgintino, Daniela aut Enthalten in Cerebrospinal fluid research London : BioMed Central, 2004 19(2022), 1 vom: 30. Aug. (DE-627)476171717 (DE-600)2171132-X 1743-8454 nnns volume:19 year:2022 number:1 day:30 month:08 https://dx.doi.org/10.1186/s12987-022-00365-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_2003 AR 19 2022 1 30 08 |
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10.1186/s12987-022-00365-5 doi (DE-627)SPR05095685X (SPR)s12987-022-00365-5-e DE-627 ger DE-627 rakwb eng Errede, Mariella verfasserin aut Microglia-derived CCL2 has a prime role in neocortex neuroinflammation 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background In myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), several areas of demyelination are detectable in mouse cerebral cortex, where neuroinflammation events are associated with scarce inflammatory infiltrates and blood–brain barrier (BBB) impairment. In this condition, the administration of mesenchymal stem cells (MSCs) controls neuroinflammation, attenuating astrogliosis and promoting the acquisition of stem cell traits by astrocytes. To contribute to the understanding of the mechanisms involved in the pathogenesis of EAE in gray matter and in the reverting effects of MSC treatment, the neocortex of EAE-affected mice was investigated by analyzing the cellular source(s) of chemokine CCL2, a molecule involved in immune cell recruitment and BBB-microvessel leakage. Methods The study was carried out by immunohistochemistry (IHC) and dual RNAscope IHC/in situ hybridization methods, using astrocyte, NG2-glia, macrophage/microglia, and microglia elective markers combined with CCL2. Results The results showed that in EAE-affected mice, hypertrophic microglia are the primary source of CCL2, surround the cortex neurons and the damaged BBB microvessels. In EAE-affected mice treated with MSCs, microgliosis appeared diminished very soon (6 h) after treatment, an observation that was long-lasting (tested after 10 days). This was associated with a reduced CCL2 expression and with apparently preserved/restored BBB features. In conclusion, the hallmark of EAE in the mouse neocortex is a condition of microgliosis characterized by high levels of CCL2 expression. Conclusions This finding supports relevant pathogenetic and clinical aspects of the human disease, while the demonstrated early control of neuroinflammation and BBB permeability exerted by treatment with MSCs may have important therapeutic implications. Experimental autoimmune encephalomyelitis (dpeaa)DE-He213 Neocortex (dpeaa)DE-He213 Microglia (dpeaa)DE-He213 CCL2 (dpeaa)DE-He213 Mesenchymal stem cells (dpeaa)DE-He213 Annese, Tiziana aut Petrosino, Valentina aut Longo, Giovanna aut Girolamo, Francesco aut de Trizio, Ignazio aut d’Amati, Antonio aut Uccelli, Antonio aut Kerlero de Rosbo, Nicole aut Virgintino, Daniela aut Enthalten in Cerebrospinal fluid research London : BioMed Central, 2004 19(2022), 1 vom: 30. Aug. (DE-627)476171717 (DE-600)2171132-X 1743-8454 nnns volume:19 year:2022 number:1 day:30 month:08 https://dx.doi.org/10.1186/s12987-022-00365-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_2003 AR 19 2022 1 30 08 |
| allfields_unstemmed |
10.1186/s12987-022-00365-5 doi (DE-627)SPR05095685X (SPR)s12987-022-00365-5-e DE-627 ger DE-627 rakwb eng Errede, Mariella verfasserin aut Microglia-derived CCL2 has a prime role in neocortex neuroinflammation 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background In myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), several areas of demyelination are detectable in mouse cerebral cortex, where neuroinflammation events are associated with scarce inflammatory infiltrates and blood–brain barrier (BBB) impairment. In this condition, the administration of mesenchymal stem cells (MSCs) controls neuroinflammation, attenuating astrogliosis and promoting the acquisition of stem cell traits by astrocytes. To contribute to the understanding of the mechanisms involved in the pathogenesis of EAE in gray matter and in the reverting effects of MSC treatment, the neocortex of EAE-affected mice was investigated by analyzing the cellular source(s) of chemokine CCL2, a molecule involved in immune cell recruitment and BBB-microvessel leakage. Methods The study was carried out by immunohistochemistry (IHC) and dual RNAscope IHC/in situ hybridization methods, using astrocyte, NG2-glia, macrophage/microglia, and microglia elective markers combined with CCL2. Results The results showed that in EAE-affected mice, hypertrophic microglia are the primary source of CCL2, surround the cortex neurons and the damaged BBB microvessels. In EAE-affected mice treated with MSCs, microgliosis appeared diminished very soon (6 h) after treatment, an observation that was long-lasting (tested after 10 days). This was associated with a reduced CCL2 expression and with apparently preserved/restored BBB features. In conclusion, the hallmark of EAE in the mouse neocortex is a condition of microgliosis characterized by high levels of CCL2 expression. Conclusions This finding supports relevant pathogenetic and clinical aspects of the human disease, while the demonstrated early control of neuroinflammation and BBB permeability exerted by treatment with MSCs may have important therapeutic implications. Experimental autoimmune encephalomyelitis (dpeaa)DE-He213 Neocortex (dpeaa)DE-He213 Microglia (dpeaa)DE-He213 CCL2 (dpeaa)DE-He213 Mesenchymal stem cells (dpeaa)DE-He213 Annese, Tiziana aut Petrosino, Valentina aut Longo, Giovanna aut Girolamo, Francesco aut de Trizio, Ignazio aut d’Amati, Antonio aut Uccelli, Antonio aut Kerlero de Rosbo, Nicole aut Virgintino, Daniela aut Enthalten in Cerebrospinal fluid research London : BioMed Central, 2004 19(2022), 1 vom: 30. Aug. (DE-627)476171717 (DE-600)2171132-X 1743-8454 nnns volume:19 year:2022 number:1 day:30 month:08 https://dx.doi.org/10.1186/s12987-022-00365-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_2003 AR 19 2022 1 30 08 |
| allfieldsGer |
10.1186/s12987-022-00365-5 doi (DE-627)SPR05095685X (SPR)s12987-022-00365-5-e DE-627 ger DE-627 rakwb eng Errede, Mariella verfasserin aut Microglia-derived CCL2 has a prime role in neocortex neuroinflammation 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background In myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), several areas of demyelination are detectable in mouse cerebral cortex, where neuroinflammation events are associated with scarce inflammatory infiltrates and blood–brain barrier (BBB) impairment. In this condition, the administration of mesenchymal stem cells (MSCs) controls neuroinflammation, attenuating astrogliosis and promoting the acquisition of stem cell traits by astrocytes. To contribute to the understanding of the mechanisms involved in the pathogenesis of EAE in gray matter and in the reverting effects of MSC treatment, the neocortex of EAE-affected mice was investigated by analyzing the cellular source(s) of chemokine CCL2, a molecule involved in immune cell recruitment and BBB-microvessel leakage. Methods The study was carried out by immunohistochemistry (IHC) and dual RNAscope IHC/in situ hybridization methods, using astrocyte, NG2-glia, macrophage/microglia, and microglia elective markers combined with CCL2. Results The results showed that in EAE-affected mice, hypertrophic microglia are the primary source of CCL2, surround the cortex neurons and the damaged BBB microvessels. In EAE-affected mice treated with MSCs, microgliosis appeared diminished very soon (6 h) after treatment, an observation that was long-lasting (tested after 10 days). This was associated with a reduced CCL2 expression and with apparently preserved/restored BBB features. In conclusion, the hallmark of EAE in the mouse neocortex is a condition of microgliosis characterized by high levels of CCL2 expression. Conclusions This finding supports relevant pathogenetic and clinical aspects of the human disease, while the demonstrated early control of neuroinflammation and BBB permeability exerted by treatment with MSCs may have important therapeutic implications. Experimental autoimmune encephalomyelitis (dpeaa)DE-He213 Neocortex (dpeaa)DE-He213 Microglia (dpeaa)DE-He213 CCL2 (dpeaa)DE-He213 Mesenchymal stem cells (dpeaa)DE-He213 Annese, Tiziana aut Petrosino, Valentina aut Longo, Giovanna aut Girolamo, Francesco aut de Trizio, Ignazio aut d’Amati, Antonio aut Uccelli, Antonio aut Kerlero de Rosbo, Nicole aut Virgintino, Daniela aut Enthalten in Cerebrospinal fluid research London : BioMed Central, 2004 19(2022), 1 vom: 30. Aug. (DE-627)476171717 (DE-600)2171132-X 1743-8454 nnns volume:19 year:2022 number:1 day:30 month:08 https://dx.doi.org/10.1186/s12987-022-00365-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_2003 AR 19 2022 1 30 08 |
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10.1186/s12987-022-00365-5 doi (DE-627)SPR05095685X (SPR)s12987-022-00365-5-e DE-627 ger DE-627 rakwb eng Errede, Mariella verfasserin aut Microglia-derived CCL2 has a prime role in neocortex neuroinflammation 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background In myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), several areas of demyelination are detectable in mouse cerebral cortex, where neuroinflammation events are associated with scarce inflammatory infiltrates and blood–brain barrier (BBB) impairment. In this condition, the administration of mesenchymal stem cells (MSCs) controls neuroinflammation, attenuating astrogliosis and promoting the acquisition of stem cell traits by astrocytes. To contribute to the understanding of the mechanisms involved in the pathogenesis of EAE in gray matter and in the reverting effects of MSC treatment, the neocortex of EAE-affected mice was investigated by analyzing the cellular source(s) of chemokine CCL2, a molecule involved in immune cell recruitment and BBB-microvessel leakage. Methods The study was carried out by immunohistochemistry (IHC) and dual RNAscope IHC/in situ hybridization methods, using astrocyte, NG2-glia, macrophage/microglia, and microglia elective markers combined with CCL2. Results The results showed that in EAE-affected mice, hypertrophic microglia are the primary source of CCL2, surround the cortex neurons and the damaged BBB microvessels. In EAE-affected mice treated with MSCs, microgliosis appeared diminished very soon (6 h) after treatment, an observation that was long-lasting (tested after 10 days). This was associated with a reduced CCL2 expression and with apparently preserved/restored BBB features. In conclusion, the hallmark of EAE in the mouse neocortex is a condition of microgliosis characterized by high levels of CCL2 expression. Conclusions This finding supports relevant pathogenetic and clinical aspects of the human disease, while the demonstrated early control of neuroinflammation and BBB permeability exerted by treatment with MSCs may have important therapeutic implications. Experimental autoimmune encephalomyelitis (dpeaa)DE-He213 Neocortex (dpeaa)DE-He213 Microglia (dpeaa)DE-He213 CCL2 (dpeaa)DE-He213 Mesenchymal stem cells (dpeaa)DE-He213 Annese, Tiziana aut Petrosino, Valentina aut Longo, Giovanna aut Girolamo, Francesco aut de Trizio, Ignazio aut d’Amati, Antonio aut Uccelli, Antonio aut Kerlero de Rosbo, Nicole aut Virgintino, Daniela aut Enthalten in Cerebrospinal fluid research London : BioMed Central, 2004 19(2022), 1 vom: 30. Aug. (DE-627)476171717 (DE-600)2171132-X 1743-8454 nnns volume:19 year:2022 number:1 day:30 month:08 https://dx.doi.org/10.1186/s12987-022-00365-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_2003 AR 19 2022 1 30 08 |
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Errede, Mariella Annese, Tiziana Petrosino, Valentina Longo, Giovanna Girolamo, Francesco de Trizio, Ignazio d’Amati, Antonio Uccelli, Antonio Kerlero de Rosbo, Nicole Virgintino, Daniela |
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microglia-derived ccl2 has a prime role in neocortex neuroinflammation |
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Microglia-derived CCL2 has a prime role in neocortex neuroinflammation |
| abstract |
Background In myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), several areas of demyelination are detectable in mouse cerebral cortex, where neuroinflammation events are associated with scarce inflammatory infiltrates and blood–brain barrier (BBB) impairment. In this condition, the administration of mesenchymal stem cells (MSCs) controls neuroinflammation, attenuating astrogliosis and promoting the acquisition of stem cell traits by astrocytes. To contribute to the understanding of the mechanisms involved in the pathogenesis of EAE in gray matter and in the reverting effects of MSC treatment, the neocortex of EAE-affected mice was investigated by analyzing the cellular source(s) of chemokine CCL2, a molecule involved in immune cell recruitment and BBB-microvessel leakage. Methods The study was carried out by immunohistochemistry (IHC) and dual RNAscope IHC/in situ hybridization methods, using astrocyte, NG2-glia, macrophage/microglia, and microglia elective markers combined with CCL2. Results The results showed that in EAE-affected mice, hypertrophic microglia are the primary source of CCL2, surround the cortex neurons and the damaged BBB microvessels. In EAE-affected mice treated with MSCs, microgliosis appeared diminished very soon (6 h) after treatment, an observation that was long-lasting (tested after 10 days). This was associated with a reduced CCL2 expression and with apparently preserved/restored BBB features. In conclusion, the hallmark of EAE in the mouse neocortex is a condition of microgliosis characterized by high levels of CCL2 expression. Conclusions This finding supports relevant pathogenetic and clinical aspects of the human disease, while the demonstrated early control of neuroinflammation and BBB permeability exerted by treatment with MSCs may have important therapeutic implications. © The Author(s) 2022 |
| abstractGer |
Background In myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), several areas of demyelination are detectable in mouse cerebral cortex, where neuroinflammation events are associated with scarce inflammatory infiltrates and blood–brain barrier (BBB) impairment. In this condition, the administration of mesenchymal stem cells (MSCs) controls neuroinflammation, attenuating astrogliosis and promoting the acquisition of stem cell traits by astrocytes. To contribute to the understanding of the mechanisms involved in the pathogenesis of EAE in gray matter and in the reverting effects of MSC treatment, the neocortex of EAE-affected mice was investigated by analyzing the cellular source(s) of chemokine CCL2, a molecule involved in immune cell recruitment and BBB-microvessel leakage. Methods The study was carried out by immunohistochemistry (IHC) and dual RNAscope IHC/in situ hybridization methods, using astrocyte, NG2-glia, macrophage/microglia, and microglia elective markers combined with CCL2. Results The results showed that in EAE-affected mice, hypertrophic microglia are the primary source of CCL2, surround the cortex neurons and the damaged BBB microvessels. In EAE-affected mice treated with MSCs, microgliosis appeared diminished very soon (6 h) after treatment, an observation that was long-lasting (tested after 10 days). This was associated with a reduced CCL2 expression and with apparently preserved/restored BBB features. In conclusion, the hallmark of EAE in the mouse neocortex is a condition of microgliosis characterized by high levels of CCL2 expression. Conclusions This finding supports relevant pathogenetic and clinical aspects of the human disease, while the demonstrated early control of neuroinflammation and BBB permeability exerted by treatment with MSCs may have important therapeutic implications. © The Author(s) 2022 |
| abstract_unstemmed |
Background In myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), several areas of demyelination are detectable in mouse cerebral cortex, where neuroinflammation events are associated with scarce inflammatory infiltrates and blood–brain barrier (BBB) impairment. In this condition, the administration of mesenchymal stem cells (MSCs) controls neuroinflammation, attenuating astrogliosis and promoting the acquisition of stem cell traits by astrocytes. To contribute to the understanding of the mechanisms involved in the pathogenesis of EAE in gray matter and in the reverting effects of MSC treatment, the neocortex of EAE-affected mice was investigated by analyzing the cellular source(s) of chemokine CCL2, a molecule involved in immune cell recruitment and BBB-microvessel leakage. Methods The study was carried out by immunohistochemistry (IHC) and dual RNAscope IHC/in situ hybridization methods, using astrocyte, NG2-glia, macrophage/microglia, and microglia elective markers combined with CCL2. Results The results showed that in EAE-affected mice, hypertrophic microglia are the primary source of CCL2, surround the cortex neurons and the damaged BBB microvessels. In EAE-affected mice treated with MSCs, microgliosis appeared diminished very soon (6 h) after treatment, an observation that was long-lasting (tested after 10 days). This was associated with a reduced CCL2 expression and with apparently preserved/restored BBB features. In conclusion, the hallmark of EAE in the mouse neocortex is a condition of microgliosis characterized by high levels of CCL2 expression. Conclusions This finding supports relevant pathogenetic and clinical aspects of the human disease, while the demonstrated early control of neuroinflammation and BBB permeability exerted by treatment with MSCs may have important therapeutic implications. © The Author(s) 2022 |
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Annese, Tiziana Petrosino, Valentina Longo, Giovanna Girolamo, Francesco de Trizio, Ignazio d’Amati, Antonio Uccelli, Antonio Kerlero de Rosbo, Nicole Virgintino, Daniela |
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