Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1

<p<Abstract</p< <p<Background</p< <p<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.</p< <p<Methods</p< <p<Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of MOG<sub<35-55 </sub<in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with MOG<sub<33-55 </sub<for 14 days were re-stimulated <it<in vitro </it<with MOG<sub<33-55 </sub<(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.</p< <p<Results</p< <p<Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of MOG<sub<35-55</sub<-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 <it<in vitro </it<following stimulation with MOG<sub<35-55 </sub<showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells.</p< <p<Conclusion</p< <p<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.</p< Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Flower Rod J [verfasserIn] Perretti Mauro [verfasserIn] Wood Elisabeth G [verfasserIn] Maione Francesco [verfasserIn] Iqbal Asif J [verfasserIn] Paschalidis Nikolaos [verfasserIn] D'Acquisto Fulvio [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2009

Übergeordnetes Werk:	In: Journal of Neuroinflammation - BMC, 2004, 6(2009), 1, p 33
Übergeordnetes Werk:	volume:6 ; year:2009 ; number:1, p 33

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1742-2094-6-33

Katalog-ID:	DOAJ026275058

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allfields	10.1186/1742-2094-6-33 doi (DE-627)DOAJ026275058 (DE-599)DOAJe8c3c0f1c56b4a4ca590ded3c7cefd56 DE-627 ger DE-627 rakwb eng RC346-429 Flower Rod J verfasserin aut Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<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.</p< <p<Methods</p< <p<Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of MOG<sub<35-55 </sub<in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with MOG<sub<33-55 </sub<for 14 days were re-stimulated <it<in vitro </it<with MOG<sub<33-55 </sub<(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.</p< <p<Results</p< <p<Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of MOG<sub<35-55</sub<-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 <it<in vitro </it<following stimulation with MOG<sub<35-55 </sub<showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells.</p< <p<Conclusion</p< <p<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.</p< Neurology. Diseases of the nervous system Perretti Mauro verfasserin aut Wood Elisabeth G verfasserin aut Maione Francesco verfasserin aut Iqbal Asif J verfasserin aut Paschalidis Nikolaos verfasserin aut D'Acquisto Fulvio verfasserin aut In Journal of Neuroinflammation BMC, 2004 6(2009), 1, p 33 (DE-627)391784781 (DE-600)2156455-3 17422094 nnns volume:6 year:2009 number:1, p 33 https://doi.org/10.1186/1742-2094-6-33 kostenfrei https://doaj.org/article/e8c3c0f1c56b4a4ca590ded3c7cefd56 kostenfrei http://www.jneuroinflammation.com/content/6/1/33 kostenfrei https://doaj.org/toc/1742-2094 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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, p 33
spelling	10.1186/1742-2094-6-33 doi (DE-627)DOAJ026275058 (DE-599)DOAJe8c3c0f1c56b4a4ca590ded3c7cefd56 DE-627 ger DE-627 rakwb eng RC346-429 Flower Rod J verfasserin aut Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<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.</p< <p<Methods</p< <p<Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of MOG<sub<35-55 </sub<in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with MOG<sub<33-55 </sub<for 14 days were re-stimulated <it<in vitro </it<with MOG<sub<33-55 </sub<(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.</p< <p<Results</p< <p<Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of MOG<sub<35-55</sub<-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 <it<in vitro </it<following stimulation with MOG<sub<35-55 </sub<showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells.</p< <p<Conclusion</p< <p<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.</p< Neurology. Diseases of the nervous system Perretti Mauro verfasserin aut Wood Elisabeth G verfasserin aut Maione Francesco verfasserin aut Iqbal Asif J verfasserin aut Paschalidis Nikolaos verfasserin aut D'Acquisto Fulvio verfasserin aut In Journal of Neuroinflammation BMC, 2004 6(2009), 1, p 33 (DE-627)391784781 (DE-600)2156455-3 17422094 nnns volume:6 year:2009 number:1, p 33 https://doi.org/10.1186/1742-2094-6-33 kostenfrei https://doaj.org/article/e8c3c0f1c56b4a4ca590ded3c7cefd56 kostenfrei http://www.jneuroinflammation.com/content/6/1/33 kostenfrei https://doaj.org/toc/1742-2094 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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, p 33
allfields_unstemmed	10.1186/1742-2094-6-33 doi (DE-627)DOAJ026275058 (DE-599)DOAJe8c3c0f1c56b4a4ca590ded3c7cefd56 DE-627 ger DE-627 rakwb eng RC346-429 Flower Rod J verfasserin aut Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<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.</p< <p<Methods</p< <p<Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of MOG<sub<35-55 </sub<in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with MOG<sub<33-55 </sub<for 14 days were re-stimulated <it<in vitro </it<with MOG<sub<33-55 </sub<(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.</p< <p<Results</p< <p<Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of MOG<sub<35-55</sub<-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 <it<in vitro </it<following stimulation with MOG<sub<35-55 </sub<showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells.</p< <p<Conclusion</p< <p<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.</p< Neurology. Diseases of the nervous system Perretti Mauro verfasserin aut Wood Elisabeth G verfasserin aut Maione Francesco verfasserin aut Iqbal Asif J verfasserin aut Paschalidis Nikolaos verfasserin aut D'Acquisto Fulvio verfasserin aut In Journal of Neuroinflammation BMC, 2004 6(2009), 1, p 33 (DE-627)391784781 (DE-600)2156455-3 17422094 nnns volume:6 year:2009 number:1, p 33 https://doi.org/10.1186/1742-2094-6-33 kostenfrei https://doaj.org/article/e8c3c0f1c56b4a4ca590ded3c7cefd56 kostenfrei http://www.jneuroinflammation.com/content/6/1/33 kostenfrei https://doaj.org/toc/1742-2094 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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, p 33
allfieldsGer	10.1186/1742-2094-6-33 doi (DE-627)DOAJ026275058 (DE-599)DOAJe8c3c0f1c56b4a4ca590ded3c7cefd56 DE-627 ger DE-627 rakwb eng RC346-429 Flower Rod J verfasserin aut Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<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.</p< <p<Methods</p< <p<Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of MOG<sub<35-55 </sub<in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with MOG<sub<33-55 </sub<for 14 days were re-stimulated <it<in vitro </it<with MOG<sub<33-55 </sub<(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.</p< <p<Results</p< <p<Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of MOG<sub<35-55</sub<-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 <it<in vitro </it<following stimulation with MOG<sub<35-55 </sub<showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells.</p< <p<Conclusion</p< <p<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.</p< Neurology. Diseases of the nervous system Perretti Mauro verfasserin aut Wood Elisabeth G verfasserin aut Maione Francesco verfasserin aut Iqbal Asif J verfasserin aut Paschalidis Nikolaos verfasserin aut D'Acquisto Fulvio verfasserin aut In Journal of Neuroinflammation BMC, 2004 6(2009), 1, p 33 (DE-627)391784781 (DE-600)2156455-3 17422094 nnns volume:6 year:2009 number:1, p 33 https://doi.org/10.1186/1742-2094-6-33 kostenfrei https://doaj.org/article/e8c3c0f1c56b4a4ca590ded3c7cefd56 kostenfrei http://www.jneuroinflammation.com/content/6/1/33 kostenfrei https://doaj.org/toc/1742-2094 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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, p 33
allfieldsSound	10.1186/1742-2094-6-33 doi (DE-627)DOAJ026275058 (DE-599)DOAJe8c3c0f1c56b4a4ca590ded3c7cefd56 DE-627 ger DE-627 rakwb eng RC346-429 Flower Rod J verfasserin aut Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<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.</p< <p<Methods</p< <p<Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of MOG<sub<35-55 </sub<in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with MOG<sub<33-55 </sub<for 14 days were re-stimulated <it<in vitro </it<with MOG<sub<33-55 </sub<(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.</p< <p<Results</p< <p<Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of MOG<sub<35-55</sub<-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 <it<in vitro </it<following stimulation with MOG<sub<35-55 </sub<showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells.</p< <p<Conclusion</p< <p<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.</p< Neurology. Diseases of the nervous system Perretti Mauro verfasserin aut Wood Elisabeth G verfasserin aut Maione Francesco verfasserin aut Iqbal Asif J verfasserin aut Paschalidis Nikolaos verfasserin aut D'Acquisto Fulvio verfasserin aut In Journal of Neuroinflammation BMC, 2004 6(2009), 1, p 33 (DE-627)391784781 (DE-600)2156455-3 17422094 nnns volume:6 year:2009 number:1, p 33 https://doi.org/10.1186/1742-2094-6-33 kostenfrei https://doaj.org/article/e8c3c0f1c56b4a4ca590ded3c7cefd56 kostenfrei http://www.jneuroinflammation.com/content/6/1/33 kostenfrei https://doaj.org/toc/1742-2094 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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, p 33
language	English
source	In Journal of Neuroinflammation 6(2009), 1, p 33 volume:6 year:2009 number:1, p 33
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authorswithroles_txt_mv	Flower Rod J @@aut@@ Perretti Mauro @@aut@@ Wood Elisabeth G @@aut@@ Maione Francesco @@aut@@ Iqbal Asif J @@aut@@ Paschalidis Nikolaos @@aut@@ D'Acquisto Fulvio @@aut@@
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issn	17422094
topic_title	RC346-429 Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1
topic	misc RC346-429 misc Neurology. Diseases of the nervous system
topic_unstemmed	misc RC346-429 misc Neurology. Diseases of the nervous system
topic_browse	misc RC346-429 misc Neurology. Diseases of the nervous system
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title	Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1
ctrlnum	(DE-627)DOAJ026275058 (DE-599)DOAJe8c3c0f1c56b4a4ca590ded3c7cefd56
title_full	Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1
author_sort	Flower Rod J
journal	Journal of Neuroinflammation
journalStr	Journal of Neuroinflammation
callnumber-first-code	R
lang_code	eng
isOA_bool	true
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publishDateSort	2009
contenttype_str_mv	txt
author_browse	Flower Rod J Perretti Mauro Wood Elisabeth G Maione Francesco Iqbal Asif J Paschalidis Nikolaos D'Acquisto Fulvio
container_volume	6
class	RC346-429
format_se	Elektronische Aufsätze
author-letter	Flower Rod J
doi_str_mv	10.1186/1742-2094-6-33
author2-role	verfasserin
title_sort	modulation of experimental autoimmune encephalomyelitis by endogenous annexin a1
callnumber	RC346-429
title_auth	Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1
abstract	<p<Abstract</p< <p<Background</p< <p<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.</p< <p<Methods</p< <p<Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of MOG<sub<35-55 </sub<in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with MOG<sub<33-55 </sub<for 14 days were re-stimulated <it<in vitro </it<with MOG<sub<33-55 </sub<(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.</p< <p<Results</p< <p<Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of MOG<sub<35-55</sub<-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 <it<in vitro </it<following stimulation with MOG<sub<35-55 </sub<showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells.</p< <p<Conclusion</p< <p<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.</p<
abstractGer	<p<Abstract</p< <p<Background</p< <p<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.</p< <p<Methods</p< <p<Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of MOG<sub<35-55 </sub<in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with MOG<sub<33-55 </sub<for 14 days were re-stimulated <it<in vitro </it<with MOG<sub<33-55 </sub<(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.</p< <p<Results</p< <p<Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of MOG<sub<35-55</sub<-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 <it<in vitro </it<following stimulation with MOG<sub<35-55 </sub<showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells.</p< <p<Conclusion</p< <p<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.</p<
abstract_unstemmed	<p<Abstract</p< <p<Background</p< <p<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.</p< <p<Methods</p< <p<Male control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 μg of MOG<sub<35-55 </sub<in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with MOG<sub<33-55 </sub<for 14 days were re-stimulated <it<in vitro </it<with MOG<sub<33-55 </sub<(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.</p< <p<Results</p< <p<Our results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of MOG<sub<35-55</sub<-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 <it<in vitro </it<following stimulation with MOG<sub<35-55 </sub<showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells.</p< <p<Conclusion</p< <p<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.</p<
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container_issue	1, p 33
title_short	Modulation of experimental autoimmune encephalomyelitis by endogenous Annexin A1
url	https://doi.org/10.1186/1742-2094-6-33 https://doaj.org/article/e8c3c0f1c56b4a4ca590ded3c7cefd56 http://www.jneuroinflammation.com/content/6/1/33 https://doaj.org/toc/1742-2094
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author2	Perretti Mauro Wood Elisabeth G Maione Francesco Iqbal Asif J Paschalidis Nikolaos D'Acquisto Fulvio
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up_date	2024-07-03T20:03:48.331Z
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