LAT regulates γδ T cell homeostasis and differentiation

摘要

LAT (linker for activation of T cells) is essential for T cell receptor signaling. Mice homozygous for a mutation of the three C-terminal LAT tyrosine residues showed a block in αβ T cell development and a partially impaired γδ T cell development. Without intentional immunization, they accumulated γδ T cells in the spleen and lymph nodes that chronically produced T helper type 2 cytokines in large amounts, and caused the maturation of plasma cells secreting immunoblobulin E (IgE) and IgG1. These effects are very similar to that triggered in the αβ lineage by a mutation involving a distinct LAT tyrosine. Thus, LAT is an essential regulatory of T cell homeostasis and terminal differentiation.