Susceptibility to experimental autoimmune encephalomyelitis is associated with altered B-cell subsets distribution and decreased serum BAFF levels.
Immunol Lett
; 135(1-2): 108-17, 2011 Mar 30.
Article
em En
| MEDLINE
| ID: mdl-20946917
ABSTRACT
B cells possess the ability to regulate either pathogenic or protective events in several autoimmune diseases such as multiple sclerosis (MS) and its experimental model, experimental autoimmune encephalomyelitis (EAE). Given the extensive use of B-cell-targeting treatments, it appears crucial to more precisely define the dual role of B cells in the progression of the disease. In the present study, we explored the impact of EAE induction on the distribution of potential regulatory B-cell subsets (CD5(+) B1a, marginal zone and transitional 2 B cells) over critical time points in the relapsing-remitting EAE model, SJL/J (H2s). The same approach was carried out in B10.S mice that are resistant to EAE induction, (H2s). The comparative data obtained from these experiments showed that the homeostasis of the regulatory B-cell subsets is altered during the EAE preclinical and acute phases. These observations were associated with a distortion of the BAFF response. All these data suggest the existence of a close relationship between B-cell homeostasis, BAFF response and the susceptibility to develop EAE.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Subpopulações de Linfócitos B
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Encefalomielite Autoimune Experimental
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Fator Ativador de Células B
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Esclerose Múltipla
Tipo de estudo:
Prognostic_studies
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Risk_factors_studies
Limite:
Animals
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Humans
Idioma:
En
Revista:
Immunol Lett
Ano de publicação:
2011
Tipo de documento:
Article