CD4(+) T cell survival is not directly linked to self-MHC-induced TCR signaling

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 .