Altered expression of Fcgamma and complement receptors on B cells in systemic lupus erythematosus.
Ann N Y Acad Sci
; 1108: 183-92, 2007 Jun.
Article
en En
| MEDLINE
| ID: mdl-17893984
ABSTRACT
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by B cell hyper-reactivity, autoantibody production, immune complex (IC) deposition, and multiple organ damage. The contribution of IC and B cell-mediated changes in the pathogenesis of SLE is well established, however, the exact role of IC-binding receptors expressed on B cells, Fcgamma receptors, and complement receptors CR1 and CR2 in these pathological processes is unclear. Development of lupus-like symptoms in mice defective for the inhibitory Fc-gammaRIIb and genetic association of certain FcgammaR genes with SLE demonstrate a significant role for these receptors but reports indicating alterations of Fcgamma or complement receptor-mediated B cell functions in human SLE are relatively few. The present review highlights a selected set of data including our own discussing the significance of animal models, genetics, and functional alterations of these IC-binding receptors in the etiopathogenesis of SLE.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Linfocitos B
/
Receptores de Complemento
/
Receptores de IgG
/
Lupus Eritematoso Sistémico
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Ann N Y Acad Sci
Año:
2007
Tipo del documento:
Article
País de afiliación:
Hungria