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,
*
Institut National de la Santé et de la Recherche Médicale, Unité 463, Institut de Biologie, Nantes, France;
Centre d’Immunologie, Institut National de la Santé et de la Recherche Médicale/Centre National de la Recherche Scientifique de Marseille Luminy, Marseille, France;
Institut Universitaire de France, Paris, France;
§
Immunotech SA, Marseille, France; and
¶
Istituto di Istologia, Universita di Genoa, Genoa, Italy
A small fraction of T cells expresses killer-cell Ig-like receptors
(KIR), a family of MHC class I-specific receptors that can modulate
TCR-dependent activation of effector functions. Although
KIR+ cells are enriched within Ag-experienced T cell
subsets, the precise relationships between KIR+ and
KIR- T cells and the stage of KIR induction on these
lymphocytes remain unclear. In this study, we compared
KIR- and KIR+ 
T cell clones, sorted by
means of the CD158b (KIR2DL2/KIR2DL3/KIR2DS2) specific mAb GL183. We
isolated several pairs of CD158b+ and CD158b-
T cell clones sharing identical productive and nonproductive TCR
transcripts. We showed that expression of functional KIR on T cells is
regulated after termination of TCR rearrangements. Transcriptional
regulation of KIR genes was documented in multiple T
cell clones generated from the same donor, and the presence of KIR
transcripts was also detected in KIR- T cells. These
results document a complex regulation of KIR expression in T cells at
both pre and posttranscriptional levels, under the control of yet
undefined signals provided in vivo.
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