Nature Immunology
1, 329 - 335 (2000)
doi:10.1038/79783
CD4+ T cell survival is not directly linked to self-MHC−induced TCR signalingJeffrey R. Dorfman2, Irena  tefanová2, Koji Yasutomo3
& Ronald N. Germain11
Lymphocyte Biology Section, Laboratory of Immunology, Building 10 Room 11N311, National Institutes of Health, Bethesda, MD 20892, USA. 2
These authors contributed equally to this work. 3
Present address: Department of Pediatrics, School of Medicine, University of Tokushima, Kuramoto 3, Tokushima 770, Japan.
Correspondence should be addressed to Ronald N. Germain ronald_germain@nih.govT 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 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 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.
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