LAT is essential for Fc(epsilon)RI-mediated mast cell activation.
Immunity
; 12(5): 525-35, 2000 May.
Article
em En
| MEDLINE
| ID: mdl-10843385
ABSTRACT
The linker molecule LAT is a substrate of the tyrosine kinases activated following TCR engagement of T cells. LAT is also expressed in platelets, NK, and mast cells. Although LAT-deficient mice contain normal numbers of mast cells, we found that LAT-deficient mice were resistant to IgE-mediated passive systemic anaphylaxis. LAT-deficient bone marrow-derived mast cells (BMMC) showed normal growth and development. Whereas tyrosine phosphorylation of Fc(epsilon)RI, Syk, and Vav was intact in LAT-deficient BMMCs following Fc(epsilon)RI engagement, tyrosine phosphorylation of SLP-76, PLC-gamma1, and PLC-gamma2 and calcium mobilization were dramatically reduced. LAT-deficient BMMCs also exhibited profound defects in activation of MAPK, degranulation, and cytokine production after Fc(epsilon)RI cross-linking. These results show that LAT plays a critical role in Fc(epsilon)RI-mediated signaling in mast cells.
Buscar no Google
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Fosfoproteínas
/
Proteínas de Transporte
/
Receptores de IgE
/
Proteínas Adaptadoras de Transdução de Sinal
/
Mastócitos
Limite:
Animals
Idioma:
En
Revista:
Immunity
Ano de publicação:
2000
Tipo de documento:
Article