T cell receptor (TCR) signaling triggered by recognition of self-major hist
ocompatibility complex (MHC) ligands has been proposed to maintain the viab
ility of naive T cells and to provoke their proliferation in T cell-deficie
nt hosts. Consistent with this, the partially phosphorylated state of TCR z
eta chains in naive CD4(+) and CD8(+) T tells in vivo was found to be activ
ely maintained by TCR interactions with specific peptide-containing MHC mol
ecules,TCR ligand-dependent phosphorylation of TCR zeta was lost within one
day of cell transfer into MHC-deficient hosts, yet the survival of transfe
rred CD4(+) lymphocytes was the same in recipients with or without MHC clas
s II expression for one month. Thus, despite clear evidence for TCR signali
ng in nonactivated naive T cells, these data argue against the concept that
such signaling plays a predominant role in determining lymphocyte lifespan
.