A mechanism for expansion of regulatory T-cell repertoire and its role in self-tolerance.

Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14740%2F15%3A00085160" target="_blank" >RIV/00216224:14740/15:00085160 - isvavai.cz</a>
Result on the web
<a href="http://www.nature.com/doifinder/10.1038/nature16141" target="_blank" >http://www.nature.com/doifinder/10.1038/nature16141</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1038/nature16141" target="_blank" >10.1038/nature16141</a>

Result language
angličtina
Original language name
A mechanism for expansion of regulatory T-cell repertoire and its role in self-tolerance.
Original language description
T-cell receptor (TCR) signalling has a key role in determining T-cell fate. Precursor cells expressing TCRs within a certain low-affinity range for complexes of self-peptide and major histocompatibility complex (MHC) undergo positive selection and differentiate into naive T cells expressing a highly diverse self-MHC-restricted TCR repertoire. In contrast, precursors displaying TCRs with a high affinity for 'self' are either eliminated through TCR-agonist-induced apoptosis (negative selection) or restrained by regulatory T (Treg) cells, whose differentiation and function are controlled by the X-chromosome-encoded transcription factor Foxp3 (reviewed in ref. 2). Foxp3 is expressed in a fraction of self-reactive T cells that escape negative selection in response to agonist-driven TCR signals combined with interleukin 2 (IL-2) receptor signalling.
Czech name
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Czech description
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Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
FD - Oncology and haematology
OECD FORD branch
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Project
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Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year
2015
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

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