Título:
|
Passive experimental autoimmune encephalomyelitis in C57BL/6 with MOG: evidence of involvement of B cells
|
Autor/a:
|
Mannara, F.; Valente, Tony; Saura Martí, Josep; Graus Ribas, Francesc; Saiz Hinajeros, Albert; Moreno, B.
|
Otros autores:
|
Universitat de Barcelona |
Abstract:
|
Experimental autoimmune encephalomyelitis (EAE) is the most relevant animal model to study demyelinating diseases such as multiple sclerosis. EAE can be induced by active (active EAE) or passive (at-EAE) transfer of activated T cells in several species and strains of rodents. However, histological features of at-EAE model in C57BL/6 are poorly described. The aim of this study was to characterize the neuroinflammatory and neurodegenerative responses of at-EAE in C57BL/6 mice by histological techniques and compare them with that observed in the active EAE model. To develop the at-EAE, splenocytes from active EAE female mice were harvested and cultured in presence of MOG 35-55 and IL-12, and then injected intraperitoneally in recipient female C57BL6/J mice. In both models, the development of EAE was similar except for starting before the onset of symptoms and presenting a higher EAE cumulative score in the at-EAE model. Spinal cord histological examination revealed an increased glial activation as well as more extensive demyelinating areas in the at-EAE than in the active EAE model. Although inflammatory infiltrates composed by macrophages and T lymphocytes were found in the spinal cord and brain of both models, B lymphocytes were significantly increased in the at-EAE model. The co-localization of these B cells with IgG and their predominant distribution in areas of demyelination would suggest that IgG-secreting B cells are involved in the neurodegenerative processes associated with at-EAE. |
Materia(s):
|
-Malalties neurodegeneratives -Cèl·lules B -Encefalomielitis -Neurodegenerative diseases -B cells -Encephalomyelitis |
Derechos:
|
cc-by (c) Mannara et al., 2012
http://creativecommons.org/licenses/by/3.0/es |
Tipo de documento:
|
Artículo Artículo - Versión publicada |
Editor:
|
Public Library of Science (PLoS)
|
Compartir:
|
|