IL-4 inhibits mouse mast cell Fc epsilonRI expression through a STAT6-dependent mechanism.
J Immunol
; 161(12): 6915-23, 1998 Dec 15.
Article
en En
| MEDLINE
| ID: mdl-9862725
Mast cell activation by IgE-mediated stimuli is a central event in atopic disease. The regulation of the mast cell high affinity receptor, Fc epsilonRI, is poorly understood. We show that IL-4 can inhibit Fc epsilonRI expression on mouse bone marrow-derived mast cells and fetal liver-derived mast cell progenitors. This effect could be observed at 2.5 ng/ml IL-4 and was dose dependent. IL-4-mediated inhibition of cultured BMMC required 4 days of stimulation and was sustained at maximum levels for at least 21 days. The inhibition of Fc epsilonRI expression resulted in decreased sensitivity to IgE-mediated stimulation, as measured by serotonin release, and the induction of mRNA for IL-4, IL-5, IL-6, and IL-13. Additionally, IL-4 could abrogate the IgE-mediated increase in Fc epsilonRI expression. Lastly, IL-4-mediated inhibition was dependent upon expression of the STAT6 transcription factor, as STAT6-deficient bone marrow-derived mast cells did not decrease Fc epsilonRI levels in response to IL-4. These data argue for a homeostatic role of IL-4 in the regulation of Fc epsilonRI expression, a role that could be critical to understanding atopic disease.
Buscar en Google
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Transcripción Genética
/
Transactivadores
/
Regulación de la Expresión Génica
/
Interleucina-4
/
Receptores de IgE
/
Hipersensibilidad Inmediata
/
Mastocitos
Límite:
Animals
Idioma:
En
Revista:
J Immunol
Año:
1998
Tipo del documento:
Article
País de afiliación:
Estados Unidos
Pais de publicación:
Estados Unidos