Deficiency in CD22, a B cell-specific inhibitory receptor, is sufficient to predispose to development of high affinity autoantibodies.
J Exp Med
; 189(8): 1307-13, 1999 Apr 19.
Article
em En
| MEDLINE
| ID: mdl-10209047
ABSTRACT
CD22 is a B cell-specific transmembrane glycoprotein that acts to dampen signals generated through the B cell antigen receptor (BCR) B cells from CD22-deficient mice give increased Ca2+ fluxes on BCR ligation. Here we show that this B cell hyperresponsiveness correlates with the development of autoantibodies. After the age of eight months, CD22-deficient mice developed high titers of serum IgG directed against double-stranded DNA; these antibodies were of multiclonal origin, somatically mutated, and high affinity. Increased titers of antibodies to cardiolipin and myeloperoxidase were also noted. The results demonstrate that a single gene defect exclusive to B lymphocytes is, without additional contrivance, sufficient to trigger autoantibody development in a large proportion of aging animals. Thus, CD22 might have evolved specifically to regulate B cell triggering thresholds for the avoidance of autoimmunity.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Autoanticorpos
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Linfócitos B
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Antígenos de Diferenciação de Linfócitos B
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Antígenos CD
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Moléculas de Adesão Celular
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Receptores de Superfície Celular
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Lectinas
Limite:
Animals
Idioma:
En
Revista:
J Exp Med
Ano de publicação:
1999
Tipo de documento:
Article
País de afiliação:
Reino Unido