Stimulation of the T-cell antigen receptor (TCR) leads to the activation of 
signaling pathways that are essential for T-cell development and the response of 
mature T cells to antigens. The TCR has no intrinsic catalytic activity, but TCR 
engagement results in tyrosine phosphorylation of downstream targets by 
non-receptor tyrosine kinases. Three families of tyrosine kinases have long been 
recognized to play critical roles in TCR-dependent signaling. They are the Src, 
zeta-associated protein of 70 kDa, and Tec families of kinases. More recently, 
the Abelson (Abl) tyrosine kinases have been shown to be activated by TCR 
engagement and to be required for maximal TCR signaling. Using T-cell 
conditional knockout mice deficient for Abl family kinases, Abl (Abl1) and 
Abl-related gene (Arg) (Abl2), it was recently shown that loss of Abl kinases 
results in defective T-cell development and a partial block in the transition to 
the CD4(+)CD8(+) stage. Abl/Arg double null T cells exhibit impaired TCR-induced 
signaling, proliferation, and cytokine production. Moreover, conditional 
knockout mice lacking Abl and Arg in T cells exhibit impaired CD8(+) T-cell 
expansion in vivo upon Listeria monocytogenes infection. Thus, Abl kinase 
signaling is required for both T-cell development and mature T-cell function.