NDLI: Contribution of TCR signaling strength to CD8+ T cell peripheral tolerance mechanisms.

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Contribution of TCR signaling strength to CD8+ T cell peripheral tolerance mechanisms.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Smith, Trevor R. F. Verdeil, Gregory Sherman, Linda A. Marquardt, Kristi
Description	Author Affiliation: Smith TR ( Department of Immunology and Microbial Sciences, The Scripps Research Institute, La Jolla, CA 92037.); Verdeil G ( Department of Immunology and Microbial Sciences, The Scripps Research Institute, La Jolla, CA 92037.); Marquardt K ( Department of Immunology and Microbial Sciences, The Scripps Research Institute, La Jolla, CA 92037.); Sherman LA ( Department of Immunology and Microbial Sciences, The Scripps Research Institute, La Jolla, CA 92037 lsherman@scripps.edu.)
Abstract	Peripheral tolerance mechanisms are in place to prevent T cells from mediating aberrant immune responses directed against self and environmental Ags. Mechanisms involved in the induction of peripheral tolerance include T cell-intrinsic pathways, such as anergy or deletion, or exogenous tolerance mediated by regulatory T cells. We have previously shown that the density of peptide-MHC class I recognized by the TCR determines whether CD8(+) T cells undergo anergy or deletion. Specifically, using a TCR-transgenic CD8(+) T cell model, we demonstrated that persistent peripheral exposure to low- or high-dose peptides in the absence of inflammatory signals resulted in clonal deletion or anergy of the T cell, respectively. In this study, by altering the affinity of the peptide-MHC tolerogen for TCR, we have confirmed that this mechanism is dependent on the level of TCR signaling that the CD8(+) T cell receives. Using altered peptide ligands (APLs) displaying high TCR affinities, we show that increasing the TCR signaling favors anergy induction. Conversely, using APLs displaying a decreased TCR affinity tilted our system in the direction of deletional tolerance. We demonstrate how differential peripheral CD8(+) T cell tolerance mechanisms are controlled by both the potency and density of MHC class I-peptide tolerogen.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1401194
Journal	The Journal of Immunology
Issue Number	7
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens Immunology Cd8-positive T-lymphocytes Histocompatibility Antigens Class I Immune Tolerance Physiology Peptides Receptors, Antigen, T-cell Animals Genetics Cytology Mice Mice, Inbred Nod Mice, Knockout Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Accumulation of serial forces on TCR and CD8 frequently applied by agonist antigenic peptides embedded in MHC molecules triggers calcium in T cells.

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Distinct mechanisms mediate naive and memory CD8 T-cell tolerance.

Self-antigen prevents CD8 T cell effector differentiation by CD134 and CD137 dual costimulation.

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Pak2 Links TCR Signaling Strength to the Development of Regulatory T Cells and Maintains Peripheral Tolerance.

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Comparison of human T cell repertoire generated in xenogeneic porcine and human thymus grafts.

Differences in antigen recognition and cytolytic activity of CD8(+) and CD8(-) T cells that express the same antigen-specific receptor.

Contribution of TCR signaling strength to CD8+ T cell peripheral tolerance mechanisms.

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Accumulation of serial forces on TCR and CD8 frequently applied by agonist antigenic peptides embedded in MHC molecules triggers calcium in T cells.

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