"Molecular and cellular pathways responsible for the Th2 lymphoproliferative disorder afflicting mice with disabled LAT adaptor"
Linker for Activation of T cells (LAT) is an adaptor that becomes activated following TCR engagement. It is essential to mediate activation of downstream signaling effectors. Mutant mice where tyrosine 136 of LAT was replaced with a phenylalanine (LatY136F mice) develop a lymphoproliferative disorder involving polyclonal CD4 effector T cells that produce massive amounts of IL-4 and trigger severe Th2 inflammation. This uncontrolled proliferation seems to be independent of MHCII-TLR interaction. In the present study, we investigate the mechanisms responsible for the development of such a lymphoproliferative disease and compare them to what occurs in normal T cells.