期刊
IMMUNITY
卷 42, 期 5, 页码 929-941出版社
CELL PRESS
DOI: 10.1016/j.immuni.2015.05.001
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资金
- Damon Runyon Cancer Research Foundation [DRR-32-15]
- NIH [U19-AI090019, U19-AI57229, 1K08DK093709-01, R00AG040149]
- Cancer Prevention and Research Institute of Texas [R1120]
- Fondation ARC pour la Recherche sur le Cancer [EML2012090493]
- Institut National du Cancer [INCa 2012-054]
- Agence Nationale de la Recherche
- George D. Smith Stanford Graduate Fellowship
- NSF Graduate Research Fellowship
- Howard Hughes Medical Institute
It has long been thought that clonal deletion efficiently removes almost all self-specific T cells from the peripheral repertoire. We found that self-peptide MHC-specific CD8(+) T cells in the blood of healthy humans were present in frequencies similar to those specific for non-self antigens. For the Y chromosome-encoded SMCY antigen, self-specific T cells exhibited only a 3-fold lower average frequency in males versus females and were anergic with respect to peptide activation, although this inhibition could be overcome by a stronger stimulus. We conclude that clonal deletion prunes but does not eliminate self-specific T cells and suggest that to do so would create holes in the repertoire that pathogens could readily exploit. In support of this hypothesis, we detected T cells specific for all 20 amino acid variants at the p5 position of a hepatitis C virus epitope in a random group of blood donors.
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