| Literature DB >> 10843385 |
S Saitoh1, R Arudchandran, T S Manetz, W Zhang, C L Sommers, P E Love, J Rivera, L E Samelson.
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.Entities:
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Year: 2000 PMID： 10843385 DOI： 10.1016/s1074-7613(00)80204-6
Source DB: PubMed Journal: Immunity ISSN： 1074-7613 Impact factor: 31.745