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Nat Immunol. 2000 Oct;1(4):329-35.

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

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Lymphocyte Biology Section, Laboratory of Immunology, Building 10 Room 11N311, National Institutes of Health, Bethesda, MD 20892, USA.


T cell receptor (TCR) signaling triggered by recognition of self-major histocompatibility complex (MHC) ligands has been proposed to maintain the viability of naïve T cells and to provoke their proliferation in T cell-deficient hosts. Consistent with this, the partially phosphorylated state of TCR zeta chains in naïve CD4+ and CD8+ T cells 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 naïve T cells, these data argue against the concept that such signaling plays a predominant role in determining lymphocyte lifespan.

[Indexed for MEDLINE]

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