Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1
Background Autoimmune diseases, like multiple sclerosis, are triggered by uncontrolled activation of cells of the immune system against self-antigen present, for instance, in the central nervous system. We have reported novel biological functions for Annexin A1, an effector of endogenous anti-inflam...
Ausführliche Beschreibung
Autor*in: |
Paschalidis, Nikolaos [verfasserIn] |
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2009 |
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© Paschalidis et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
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Übergeordnetes Werk: |
Enthalten in: Journal of neuroinflammation - London : BioMed Central, 2004, 6(2009), 1 vom: 13. Nov. |
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Übergeordnetes Werk: |
volume:6 ; year:2009 ; number:1 ; day:13 ; month:11 |
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DOI / URN: |
10.1186/1742-2094-6-33 |
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SPR029089603 |
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520 | |a Background Autoimmune diseases, like multiple sclerosis, are triggered by uncontrolled activation of cells of the immune system against self-antigen present, for instance, in the central nervous system. We have reported novel biological functions for Annexin A1, an effector of endogenous anti-inflammation, to produce positive actions on the adaptive immune system by reducing the threshold of T cell activation. In this study, we investigated the potential modulatory role of Annexin A1 in the development of experimental autoimmune encephalomyelitis, a model of multiple sclerosis. Methods Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of $ MOG_{35-55} $ in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with $ MOG_{33-55} $ for 14 days were re-stimulated in vitro with $ MOG_{33-55} $ (100 μg/ml) for 4 days and the Th1/Th17 cytokine profile measured by ELISA. Spinal cords were processed either to isolate the infiltrated T cells or fixed and stained with haematoxylin and eosin. Statistical analyses were performed using two-tailed, unpaired Student's t tests or ANOVA. Results Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of $ MOG_{35-55} $-induced EAE development in Annexin A1 null mice showed decreased signs of the disease compared to wild type mice. This defect was significant at the peak of the disease and accompanied by reduced infiltration of T cells in the spinal cord. Finally, analysis of the T cell recall response in vitro following stimulation with $ MOG_{35-55} $ showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells. Conclusion Together these findings suggest that Annexin A1 null mice have an impaired capacity to develop EAE. Furthermore strategies aiming at reducing Annexin A1 functions or expression in T cells might represent a novel therapeutic approach for multiple sclerosis. | ||
650 | 4 | |a Multiple Sclerosis |7 (dpeaa)DE-He213 | |
650 | 4 | |a Experimental Autoimmune Encephalomyelitis |7 (dpeaa)DE-He213 | |
650 | 4 | |a Spinal Cord Tissue |7 (dpeaa)DE-He213 | |
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700 | 1 | |a Iqbal, Asif J |4 aut | |
700 | 1 | |a Maione, Francesco |4 aut | |
700 | 1 | |a Wood, Elisabeth G |4 aut | |
700 | 1 | |a Perretti, Mauro |4 aut | |
700 | 1 | |a Flower, Rod J |4 aut | |
700 | 1 | |a D'Acquisto, Fulvio |4 aut | |
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10.1186/1742-2094-6-33 doi (DE-627)SPR029089603 (SPR)1742-2094-6-33-e DE-627 ger DE-627 rakwb eng Paschalidis, Nikolaos verfasserin aut Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Paschalidis et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Autoimmune diseases, like multiple sclerosis, are triggered by uncontrolled activation of cells of the immune system against self-antigen present, for instance, in the central nervous system. We have reported novel biological functions for Annexin A1, an effector of endogenous anti-inflammation, to produce positive actions on the adaptive immune system by reducing the threshold of T cell activation. In this study, we investigated the potential modulatory role of Annexin A1 in the development of experimental autoimmune encephalomyelitis, a model of multiple sclerosis. Methods Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of $ MOG_{35-55} $ in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with $ MOG_{33-55} $ for 14 days were re-stimulated in vitro with $ MOG_{33-55} $ (100 μg/ml) for 4 days and the Th1/Th17 cytokine profile measured by ELISA. Spinal cords were processed either to isolate the infiltrated T cells or fixed and stained with haematoxylin and eosin. Statistical analyses were performed using two-tailed, unpaired Student's t tests or ANOVA. Results Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of $ MOG_{35-55} $-induced EAE development in Annexin A1 null mice showed decreased signs of the disease compared to wild type mice. This defect was significant at the peak of the disease and accompanied by reduced infiltration of T cells in the spinal cord. Finally, analysis of the T cell recall response in vitro following stimulation with $ MOG_{35-55} $ showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells. Conclusion Together these findings suggest that Annexin A1 null mice have an impaired capacity to develop EAE. Furthermore strategies aiming at reducing Annexin A1 functions or expression in T cells might represent a novel therapeutic approach for multiple sclerosis. Multiple Sclerosis (dpeaa)DE-He213 Experimental Autoimmune Encephalomyelitis (dpeaa)DE-He213 Spinal Cord Tissue (dpeaa)DE-He213 Hind Limb Paralysis (dpeaa)DE-He213 AnxA1 Expression (dpeaa)DE-He213 Iqbal, Asif J aut Maione, Francesco aut Wood, Elisabeth G aut Perretti, Mauro aut Flower, Rod J aut D'Acquisto, Fulvio aut Enthalten in Journal of neuroinflammation London : BioMed Central, 2004 6(2009), 1 vom: 13. Nov. (DE-627)391784781 (DE-600)2156455-3 1742-2094 nnns volume:6 year:2009 number:1 day:13 month:11 https://dx.doi.org/10.1186/1742-2094-6-33 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2009 1 13 11 |
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10.1186/1742-2094-6-33 doi (DE-627)SPR029089603 (SPR)1742-2094-6-33-e DE-627 ger DE-627 rakwb eng Paschalidis, Nikolaos verfasserin aut Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Paschalidis et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Autoimmune diseases, like multiple sclerosis, are triggered by uncontrolled activation of cells of the immune system against self-antigen present, for instance, in the central nervous system. We have reported novel biological functions for Annexin A1, an effector of endogenous anti-inflammation, to produce positive actions on the adaptive immune system by reducing the threshold of T cell activation. In this study, we investigated the potential modulatory role of Annexin A1 in the development of experimental autoimmune encephalomyelitis, a model of multiple sclerosis. Methods Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of $ MOG_{35-55} $ in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with $ MOG_{33-55} $ for 14 days were re-stimulated in vitro with $ MOG_{33-55} $ (100 μg/ml) for 4 days and the Th1/Th17 cytokine profile measured by ELISA. Spinal cords were processed either to isolate the infiltrated T cells or fixed and stained with haematoxylin and eosin. Statistical analyses were performed using two-tailed, unpaired Student's t tests or ANOVA. Results Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of $ MOG_{35-55} $-induced EAE development in Annexin A1 null mice showed decreased signs of the disease compared to wild type mice. This defect was significant at the peak of the disease and accompanied by reduced infiltration of T cells in the spinal cord. Finally, analysis of the T cell recall response in vitro following stimulation with $ MOG_{35-55} $ showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells. Conclusion Together these findings suggest that Annexin A1 null mice have an impaired capacity to develop EAE. Furthermore strategies aiming at reducing Annexin A1 functions or expression in T cells might represent a novel therapeutic approach for multiple sclerosis. Multiple Sclerosis (dpeaa)DE-He213 Experimental Autoimmune Encephalomyelitis (dpeaa)DE-He213 Spinal Cord Tissue (dpeaa)DE-He213 Hind Limb Paralysis (dpeaa)DE-He213 AnxA1 Expression (dpeaa)DE-He213 Iqbal, Asif J aut Maione, Francesco aut Wood, Elisabeth G aut Perretti, Mauro aut Flower, Rod J aut D'Acquisto, Fulvio aut Enthalten in Journal of neuroinflammation London : BioMed Central, 2004 6(2009), 1 vom: 13. Nov. (DE-627)391784781 (DE-600)2156455-3 1742-2094 nnns volume:6 year:2009 number:1 day:13 month:11 https://dx.doi.org/10.1186/1742-2094-6-33 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2009 1 13 11 |
allfields_unstemmed |
10.1186/1742-2094-6-33 doi (DE-627)SPR029089603 (SPR)1742-2094-6-33-e DE-627 ger DE-627 rakwb eng Paschalidis, Nikolaos verfasserin aut Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Paschalidis et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Autoimmune diseases, like multiple sclerosis, are triggered by uncontrolled activation of cells of the immune system against self-antigen present, for instance, in the central nervous system. We have reported novel biological functions for Annexin A1, an effector of endogenous anti-inflammation, to produce positive actions on the adaptive immune system by reducing the threshold of T cell activation. In this study, we investigated the potential modulatory role of Annexin A1 in the development of experimental autoimmune encephalomyelitis, a model of multiple sclerosis. Methods Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of $ MOG_{35-55} $ in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with $ MOG_{33-55} $ for 14 days were re-stimulated in vitro with $ MOG_{33-55} $ (100 μg/ml) for 4 days and the Th1/Th17 cytokine profile measured by ELISA. Spinal cords were processed either to isolate the infiltrated T cells or fixed and stained with haematoxylin and eosin. Statistical analyses were performed using two-tailed, unpaired Student's t tests or ANOVA. Results Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of $ MOG_{35-55} $-induced EAE development in Annexin A1 null mice showed decreased signs of the disease compared to wild type mice. This defect was significant at the peak of the disease and accompanied by reduced infiltration of T cells in the spinal cord. Finally, analysis of the T cell recall response in vitro following stimulation with $ MOG_{35-55} $ showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells. Conclusion Together these findings suggest that Annexin A1 null mice have an impaired capacity to develop EAE. Furthermore strategies aiming at reducing Annexin A1 functions or expression in T cells might represent a novel therapeutic approach for multiple sclerosis. Multiple Sclerosis (dpeaa)DE-He213 Experimental Autoimmune Encephalomyelitis (dpeaa)DE-He213 Spinal Cord Tissue (dpeaa)DE-He213 Hind Limb Paralysis (dpeaa)DE-He213 AnxA1 Expression (dpeaa)DE-He213 Iqbal, Asif J aut Maione, Francesco aut Wood, Elisabeth G aut Perretti, Mauro aut Flower, Rod J aut D'Acquisto, Fulvio aut Enthalten in Journal of neuroinflammation London : BioMed Central, 2004 6(2009), 1 vom: 13. Nov. (DE-627)391784781 (DE-600)2156455-3 1742-2094 nnns volume:6 year:2009 number:1 day:13 month:11 https://dx.doi.org/10.1186/1742-2094-6-33 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2009 1 13 11 |
allfieldsGer |
10.1186/1742-2094-6-33 doi (DE-627)SPR029089603 (SPR)1742-2094-6-33-e DE-627 ger DE-627 rakwb eng Paschalidis, Nikolaos verfasserin aut Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Paschalidis et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Autoimmune diseases, like multiple sclerosis, are triggered by uncontrolled activation of cells of the immune system against self-antigen present, for instance, in the central nervous system. We have reported novel biological functions for Annexin A1, an effector of endogenous anti-inflammation, to produce positive actions on the adaptive immune system by reducing the threshold of T cell activation. In this study, we investigated the potential modulatory role of Annexin A1 in the development of experimental autoimmune encephalomyelitis, a model of multiple sclerosis. Methods Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of $ MOG_{35-55} $ in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with $ MOG_{33-55} $ for 14 days were re-stimulated in vitro with $ MOG_{33-55} $ (100 μg/ml) for 4 days and the Th1/Th17 cytokine profile measured by ELISA. Spinal cords were processed either to isolate the infiltrated T cells or fixed and stained with haematoxylin and eosin. Statistical analyses were performed using two-tailed, unpaired Student's t tests or ANOVA. Results Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of $ MOG_{35-55} $-induced EAE development in Annexin A1 null mice showed decreased signs of the disease compared to wild type mice. This defect was significant at the peak of the disease and accompanied by reduced infiltration of T cells in the spinal cord. Finally, analysis of the T cell recall response in vitro following stimulation with $ MOG_{35-55} $ showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells. Conclusion Together these findings suggest that Annexin A1 null mice have an impaired capacity to develop EAE. Furthermore strategies aiming at reducing Annexin A1 functions or expression in T cells might represent a novel therapeutic approach for multiple sclerosis. Multiple Sclerosis (dpeaa)DE-He213 Experimental Autoimmune Encephalomyelitis (dpeaa)DE-He213 Spinal Cord Tissue (dpeaa)DE-He213 Hind Limb Paralysis (dpeaa)DE-He213 AnxA1 Expression (dpeaa)DE-He213 Iqbal, Asif J aut Maione, Francesco aut Wood, Elisabeth G aut Perretti, Mauro aut Flower, Rod J aut D'Acquisto, Fulvio aut Enthalten in Journal of neuroinflammation London : BioMed Central, 2004 6(2009), 1 vom: 13. Nov. (DE-627)391784781 (DE-600)2156455-3 1742-2094 nnns volume:6 year:2009 number:1 day:13 month:11 https://dx.doi.org/10.1186/1742-2094-6-33 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2009 1 13 11 |
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10.1186/1742-2094-6-33 doi (DE-627)SPR029089603 (SPR)1742-2094-6-33-e DE-627 ger DE-627 rakwb eng Paschalidis, Nikolaos verfasserin aut Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Paschalidis et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Autoimmune diseases, like multiple sclerosis, are triggered by uncontrolled activation of cells of the immune system against self-antigen present, for instance, in the central nervous system. We have reported novel biological functions for Annexin A1, an effector of endogenous anti-inflammation, to produce positive actions on the adaptive immune system by reducing the threshold of T cell activation. In this study, we investigated the potential modulatory role of Annexin A1 in the development of experimental autoimmune encephalomyelitis, a model of multiple sclerosis. Methods Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of $ MOG_{35-55} $ in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with $ MOG_{33-55} $ for 14 days were re-stimulated in vitro with $ MOG_{33-55} $ (100 μg/ml) for 4 days and the Th1/Th17 cytokine profile measured by ELISA. Spinal cords were processed either to isolate the infiltrated T cells or fixed and stained with haematoxylin and eosin. Statistical analyses were performed using two-tailed, unpaired Student's t tests or ANOVA. Results Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of $ MOG_{35-55} $-induced EAE development in Annexin A1 null mice showed decreased signs of the disease compared to wild type mice. This defect was significant at the peak of the disease and accompanied by reduced infiltration of T cells in the spinal cord. Finally, analysis of the T cell recall response in vitro following stimulation with $ MOG_{35-55} $ showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells. Conclusion Together these findings suggest that Annexin A1 null mice have an impaired capacity to develop EAE. Furthermore strategies aiming at reducing Annexin A1 functions or expression in T cells might represent a novel therapeutic approach for multiple sclerosis. Multiple Sclerosis (dpeaa)DE-He213 Experimental Autoimmune Encephalomyelitis (dpeaa)DE-He213 Spinal Cord Tissue (dpeaa)DE-He213 Hind Limb Paralysis (dpeaa)DE-He213 AnxA1 Expression (dpeaa)DE-He213 Iqbal, Asif J aut Maione, Francesco aut Wood, Elisabeth G aut Perretti, Mauro aut Flower, Rod J aut D'Acquisto, Fulvio aut Enthalten in Journal of neuroinflammation London : BioMed Central, 2004 6(2009), 1 vom: 13. Nov. (DE-627)391784781 (DE-600)2156455-3 1742-2094 nnns volume:6 year:2009 number:1 day:13 month:11 https://dx.doi.org/10.1186/1742-2094-6-33 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2009 1 13 11 |
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Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1 |
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Background Autoimmune diseases, like multiple sclerosis, are triggered by uncontrolled activation of cells of the immune system against self-antigen present, for instance, in the central nervous system. We have reported novel biological functions for Annexin A1, an effector of endogenous anti-inflammation, to produce positive actions on the adaptive immune system by reducing the threshold of T cell activation. In this study, we investigated the potential modulatory role of Annexin A1 in the development of experimental autoimmune encephalomyelitis, a model of multiple sclerosis. Methods Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of $ MOG_{35-55} $ in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with $ MOG_{33-55} $ for 14 days were re-stimulated in vitro with $ MOG_{33-55} $ (100 μg/ml) for 4 days and the Th1/Th17 cytokine profile measured by ELISA. Spinal cords were processed either to isolate the infiltrated T cells or fixed and stained with haematoxylin and eosin. Statistical analyses were performed using two-tailed, unpaired Student's t tests or ANOVA. Results Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of $ MOG_{35-55} $-induced EAE development in Annexin A1 null mice showed decreased signs of the disease compared to wild type mice. This defect was significant at the peak of the disease and accompanied by reduced infiltration of T cells in the spinal cord. Finally, analysis of the T cell recall response in vitro following stimulation with $ MOG_{35-55} $ showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells. Conclusion Together these findings suggest that Annexin A1 null mice have an impaired capacity to develop EAE. Furthermore strategies aiming at reducing Annexin A1 functions or expression in T cells might represent a novel therapeutic approach for multiple sclerosis. © Paschalidis et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
abstractGer |
Background Autoimmune diseases, like multiple sclerosis, are triggered by uncontrolled activation of cells of the immune system against self-antigen present, for instance, in the central nervous system. We have reported novel biological functions for Annexin A1, an effector of endogenous anti-inflammation, to produce positive actions on the adaptive immune system by reducing the threshold of T cell activation. In this study, we investigated the potential modulatory role of Annexin A1 in the development of experimental autoimmune encephalomyelitis, a model of multiple sclerosis. Methods Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of $ MOG_{35-55} $ in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with $ MOG_{33-55} $ for 14 days were re-stimulated in vitro with $ MOG_{33-55} $ (100 μg/ml) for 4 days and the Th1/Th17 cytokine profile measured by ELISA. Spinal cords were processed either to isolate the infiltrated T cells or fixed and stained with haematoxylin and eosin. Statistical analyses were performed using two-tailed, unpaired Student's t tests or ANOVA. Results Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of $ MOG_{35-55} $-induced EAE development in Annexin A1 null mice showed decreased signs of the disease compared to wild type mice. This defect was significant at the peak of the disease and accompanied by reduced infiltration of T cells in the spinal cord. Finally, analysis of the T cell recall response in vitro following stimulation with $ MOG_{35-55} $ showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells. Conclusion Together these findings suggest that Annexin A1 null mice have an impaired capacity to develop EAE. Furthermore strategies aiming at reducing Annexin A1 functions or expression in T cells might represent a novel therapeutic approach for multiple sclerosis. © Paschalidis et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
abstract_unstemmed |
Background Autoimmune diseases, like multiple sclerosis, are triggered by uncontrolled activation of cells of the immune system against self-antigen present, for instance, in the central nervous system. We have reported novel biological functions for Annexin A1, an effector of endogenous anti-inflammation, to produce positive actions on the adaptive immune system by reducing the threshold of T cell activation. In this study, we investigated the potential modulatory role of Annexin A1 in the development of experimental autoimmune encephalomyelitis, a model of multiple sclerosis. Methods Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of $ MOG_{35-55} $ in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with $ MOG_{33-55} $ for 14 days were re-stimulated in vitro with $ MOG_{33-55} $ (100 μg/ml) for 4 days and the Th1/Th17 cytokine profile measured by ELISA. Spinal cords were processed either to isolate the infiltrated T cells or fixed and stained with haematoxylin and eosin. Statistical analyses were performed using two-tailed, unpaired Student's t tests or ANOVA. Results Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of $ MOG_{35-55} $-induced EAE development in Annexin A1 null mice showed decreased signs of the disease compared to wild type mice. This defect was significant at the peak of the disease and accompanied by reduced infiltration of T cells in the spinal cord. Finally, analysis of the T cell recall response in vitro following stimulation with $ MOG_{35-55} $ showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells. Conclusion Together these findings suggest that Annexin A1 null mice have an impaired capacity to develop EAE. Furthermore strategies aiming at reducing Annexin A1 functions or expression in T cells might represent a novel therapeutic approach for multiple sclerosis. © Paschalidis et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
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Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1 |
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Iqbal, Asif J Maione, Francesco Wood, Elisabeth G Perretti, Mauro Flower, Rod J D'Acquisto, Fulvio |
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