LAT is essential for Fc(epsilon)RI-mediated mast cell activation.

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Saitoh, S; Arudchandran, R; Manetz, TS; Zhang, W; Sommers, CL; Love, PE; Rivera, J; Samelson, LE

Published Date

  • May 2000

Published In

Volume / Issue

  • 12 / 5

Start / End Page

  • 525 - 535

PubMed ID

  • 10843385

Pubmed Central ID

  • 10843385

International Standard Serial Number (ISSN)

  • 1074-7613

Digital Object Identifier (DOI)

  • 10.1016/s1074-7613(00)80204-6

Language

  • eng

Conference Location

  • United States