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

Bertrand Huard () and Lars Karlsson
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Bertrand Huard: The R.W. Johnson Pharmaceutical Research Institute
Lars Karlsson: The R.W. Johnson Pharmaceutical Research Institute

Nature, 2000, vol. 403, issue 6767, 325-328

Abstract: 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 unclear1,2,3. 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.

Date: 2000
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DOI: 10.1038/35002105

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