T cell receptor (TCR) signaling triggered by recognition of self-major histocompatibility complex (MHC) ligands has been proposed to maintain the viability of naive T cells and to provoke their proliferation in T cell-deficient hosts. Consistent with this, the partially phosphorylated state of TCR zeta chains in naive CD4(+) and CD8(+) T tells in vivo was found to be actively maintained by TCR interactions with specific peptide-containing MHC molecules,TCR ligand-dependent phosphorylation of TCR zeta was lost within one day of cell transfer into MHC-deficient hosts, yet the survival of transferred CD4(+) lymphocytes was the same in recipients with or without MHC class II expression for one month. Thus, despite clear evidence for TCR signaling in nonactivated naive T cells, these data argue against the concept that such signaling plays a predominant role in determining lymphocyte lifespan.
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