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Immunity. 2015 May 19;42(5):929-41. doi: 10.1016/j.immuni.2015.05.001.

Clonal Deletion Prunes but Does Not Eliminate Self-Specific αβ CD8(+) T Lymphocytes.

Author information

1
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA; Division of Hematology, Stanford University School of Medicine, Stanford, CA 94305, USA.
2
Department of Bioengineering, Stanford University School of Medicine, Stanford, CA 94305, USA.
3
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
4
INSERM, UMR1043, Centre de Physiopathologie de Toulouse Purpan, Toulouse, France and Université Toulouse III Paul-Sabatier, 31024 Toulouse, France.
5
Department of Pediatric Endocrinology, Stanford University School of Medicine, Stanford, CA 94305, USA.
6
Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.
7
Department of Bioengineering, Stanford University School of Medicine, Stanford, CA 94305, USA; Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
8
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA; Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: mmdavis@stanford.edu.

Abstract

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.

PMID:
25992863
PMCID:
PMC4455602
DOI:
10.1016/j.immuni.2015.05.001
[Indexed for MEDLINE]
Free PMC Article

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