C-Phycocyanin ameliorates experimental autoimmune encephalomyelitis and induces regulatory T cells

For decades Experimental Autoimmune Encephalitis (EAE) has remained as an unsurpassed multiple sclerosis (MS) animal model. C-Phycocyanin (C-Pc) has been reported to exhibit pharmacological properties that may be expected to symptomatically improve EAE and MS. However, in this paper we reveal a basi...

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Published in:International immunopharmacology Vol. 11; no. 1; pp. 29 - 38
Main Authors: Pentón-Rol, Giselle, Martínez-Sánchez, Gregorio, Cervantes-Llanos, Majel, Lagumersindez-Denis, Nielsen, Acosta-Medina, Emilio Felino, Falcón-Cama, Viviana, Alonso-Ramírez, Ruby, Valenzuela-Silva, Carmen, Rodríguez-Jiménez, Efraín, Llópiz-Arzuaga, Alexey, Marín-Prida, Javier, López-Saura, Pedro Antonio, Guillén-Nieto, Gerardo Emilio, Pentón-Arias, Eduardo
Format: Journal Article
Language:English
Published: Kidlington Elsevier B.V 2011
Elsevier
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Summary:For decades Experimental Autoimmune Encephalitis (EAE) has remained as an unsurpassed multiple sclerosis (MS) animal model. C-Phycocyanin (C-Pc) has been reported to exhibit pharmacological properties that may be expected to symptomatically improve EAE and MS. However, in this paper we reveal a basic underlying mechanism that may provide a new approach to the rationale of the overall beneficial effect of this natural antioxidant. We demonstrate that C-Pc is able to trigger mechanisms preventing or downgrading EAE expression and induces a regulatory T cell (Treg) response, in peripheral blood mononuclear cells (PBMC) from MS patients. These results agree with reports suggesting that Treg limit acute MS attacks and that C-Pc may act as a neuroprotector and thereby reverts the organic and functional damage in neurodegenerative disorders of the central nervous system (CNS). Moreover, evidence is provided on the antioxidant activity of C-Pc within the CNS, intended to improve the myelin and axonal damage of EAE induced Lewis rats. Our results indicate that specific Treg activation may represent a central and essential mechanism in supporting the therapeutic potential of C-Pc for MS and may lead to new and more effective therapies; this property would then complement and enhance other proven active principles such as interferons (IFN), giving rise to combined therapies. [Display omitted]
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ISSN:1567-5769
1878-1705
DOI:10.1016/j.intimp.2010.10.001