CD23: an overlooked regulator of allergic disease.
Curr Allergy Asthma Rep
; 7(5): 331-7, 2007 Sep.
Article
en En
| MEDLINE
| ID: mdl-17697638
ABSTRACT
Given the importance of immunoglobulin (Ig) E in mediating type I hypersensitivity, inhibiting IgE production would be a general way of controlling allergic disease. The low-affinity IgE receptor (FceRII or CD23) has long been proposed to be a natural regulator of IgE synthesis. In vivo research supporting this concept includes the observation that mice lacking CD23 have increased IgE production whereas mice overexpressing CD23 show strongly suppressed IgE responses. In addition, the finding that mice injected with monoclonal antibody directed against the coiled-coil stalk of CD23 have enhanced soluble CD23 release and increased IgE production demonstrates that full-length, trimeric CD23 is responsible for initiating an IgE inhibitory signal. The recent identification of ADAM10 (a disintegrin and metalloprotease) as the CD23 metalloprotease provides an alternative approach for designing therapies to combat allergic disease. Current data suggest that stabilizing cell-surface CD23 would be a natural means to decrease IgE synthesis and thus control type I hypersensitivity.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Inmunoglobulina E
/
Receptores de IgE
/
Hipersensibilidad
Tipo de estudio:
Prognostic_studies
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Curr Allergy Asthma Rep
Asunto de la revista:
ALERGIA E IMUNOLOGIA
Año:
2007
Tipo del documento:
Article
País de afiliación:
Estados Unidos