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(Received for publication, October 8, 1996, and in revised form, December 2, 1996)
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From the Natural killer and T cells express at their
surface, members of a multigenic family of killer cell inhibitory
receptors (KIR) for major histocompatibility complex Class I molecules.
KIR engagement leads to the inhibition of natural killer and T cell
activation programs. We investigated here the functional reconstitution
of KIR in a non-lymphoid cell type. Using stable transfection in the
RBL-2H3 mast cell line, we demonstrated that (i) KIR can inhibit signals induced by Fc
Centre d'Immunologie INSERM/CNRS de
Marseille-Luminy, Case 906, 13288 Marseille Cedex 09, France,
** Laboratoire d'Immunologie Cellulaire et Clinique, INSERM U255,
Institut Curie, Paris, 75 231 France, § Laboratoire
d'Immunologie Cellulaire, CNRS URA625, CERVI, Groupe hospitalier
Pitié-Salpêtrière, 75013 Paris, France,
¶ Istituto Nazionale per la Ricerca sul Cancro, Via R. Benzi, 10, 16132 Genova, Italy, and 
Istituto di Istologia ed Embriologia
Generale, University of Genova, Genova, 16 132 Italy
RI
or CD3
polypeptides that bear
immunoreceptor tyrosine-based activation motifs; (ii) two distinct
immunoreceptor tyrosine-based inhibition motifs-bearing receptors,
i.e. KIR and FcRIIB, use distinct inhibitory pathways
since KIR engagement inhibits the intracellular Ca2+
release from endoplasmic reticulum stores, in contrast to FcRIIB, which only inhibits extracellular Ca2+ entry; (iii) KIR
require co-ligation with an immunoreceptor tyrosine-based activation
motif-dependent receptor to mediate their inhibitory function. This latter finding is central to the mechanism by which KIR
selectively inhibit only the activatory receptors in close vicinity.
Taken together our observations also contribute to define and extend
the family of immunoreceptor tyrosine-based inhibition motif-bearing
receptors involved in the negative control of cell activation.
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