NKT cell-TCR expression activates conventional T cells in vivo, but is largely dispensable for mature NKT cell biology

Natural killer T (NKT) cell development depends on recognition of self-glycolipids via their semi-invariant Vα14i-TCR. However, to what extent TCR-mediated signals determine identity and function of mature NKT cells remains incompletely understood. To address this issue, we developed a mouse strain...

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Bibliographic Details
Published in:PLoS biology 2013-06, Vol.11 (6), p.e1001589-e1001589
Main Authors: Vahl, J Christoph, Heger, Klaus, Knies, Nathalie, Hein, Marco Y, Boon, Louis, Yagita, Hideo, Polic, Bojan, Schmidt-Supprian, Marc
Format: Article
Language:English
Subjects:
Animals
Antigens
Biology
Cell Differentiation - immunology
Cell Lineage
Cytokines
Cytokines - secretion
Gene Knock-In Techniques
Homeostasis
Immunity, Innate - immunology
Immunology
Inflammation - immunology
Inflammation - pathology
Lymphocyte Activation - immunology
Lymphocyte Count
Mice
Mice, Transgenic
Natural Killer T-Cells - cytology
Natural Killer T-Cells - immunology
Phenotype
Proteins
Receptors, Antigen, T-Cell, alpha-beta - metabolism
Signal Transduction - immunology
T cell receptors
Time Factors
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Summary:Natural killer T (NKT) cell development depends on recognition of self-glycolipids via their semi-invariant Vα14i-TCR. However, to what extent TCR-mediated signals determine identity and function of mature NKT cells remains incompletely understood. To address this issue, we developed a mouse strain allowing conditional Vα14i-TCR expression from within the endogenous Tcrα locus. We demonstrate that naïve T cells are activated upon replacement of their endogenous TCR repertoire with Vα14i-restricted TCRs, but they do not differentiate into NKT cells. On the other hand, induced TCR ablation on mature NKT cells did not affect their lineage identity, homeostasis, or innate rapid cytokine secretion abilities. We therefore propose that peripheral NKT cells become unresponsive to and thus are independent of their autoreactive TCR.
ISSN:1545-7885
1544-9173
1545-7885
DOI:10.1371/journal.pbio.1001589