KIR expression on self-reactive CD8+ T cells is controlled by T-cell receptor engagement View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2000-01

AUTHORS

Bertrand Huard, Lars Karlsson

ABSTRACT

Natural killer cell tolerance is maintained by the interaction of killer inhibitory receptors (KIRs) with self-major histocompatibility complex class I gene products. A subset of T cells also expresses inhibitory receptors, but the functional significance of these receptors on T cells is unclear. Here we show that, in the absence of T-cell receptor (TCR) engagement, KIRs expressed on CD8+ T cells are slowly downregulated by KIR ligands expressed on antigen-presenting cells. The resulting expression levels of KIR are no longer able to inhibit T-cell function. In contrast, TCR engagement sustains KIR expression, and re-induces functional levels of KIR expression after ligand-induced downregulation of KIR. Our data indicate that KIR expression on CD8+ T cells in vivo may be maintained through continuous encounters with antigen. As KIR-mediated inhibition of T-cell activation can be bypassed at high antigen concentrations, dynamic KIR expression may mediate T-cell tolerance to self-antigens by sparing self-reactive T cells, thus enabling them to mediate potentially useful immune functions to quantitatively or qualitatively different antigens. More... »

PAGES

325

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/35002105

DOI

http://dx.doi.org/10.1038/35002105

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1026970926

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/10659853


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