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Blood, Vol. 94 No. 7 (October 1), 1999:
pp. 2396-2402
Modulation of T-Cell Functions in KIR2DL3 (CD158b) Transgenic Mice
Anna Cambiaggi,
Sylvie Darche,
Sophie Guia,
Philippe Kourilsky,
Jean-Pierre Abastado, and
Eric Vivier
From the Unité de Biologie Moléculaire du Gène,
Institut Pasteur, Paris, France; the Centre d'Immunologie INSERM/CNRS
de Marseille-Luminy, Marseille, France; and the Institut Universitaire
de France, France.
In humans, a minor subset of T cells express killer cell Ig-like
receptors (KIRs) at their surface. In vitro data obtained with
KIR+   and   T-cell clones showed that
engagement of KIR molecules can extinguish T-cell activation signals
induced via the CD3/T-cell receptor (TCR) complex. We analyzed the
T-cell compartment in mice transgenic for KIR2DL3
(Tg-KIR2DL3), an inhibitory receptor for HLA-Cw3. As
expected, mixed lymphocyte reaction and anti-CD3 monoclonal antibody
(MoAb)-redirected cytotoxicity exerted by freshly isolated splenocytes
can be inhibited by engagement of transgenic KIR2DL3 molecules. In
contrast, antigen and anti-CD3 MoAb-induced cytotoxicity exerted by
alloreactive cytotoxic T lymphocytes cannot be inhibited
by KIR2DL3 engagement. In double transgenic mice, Tg-KIR2DL3 × Tg-HLA-Cw3, no alteration of thymic differentiation could be
documented. Immunization of double transgenic mice with Hen egg white
lysozime (HEL) or Pigeon Cytochrome-C (PCC) was indistinguishable from
immunization of control mice, as judged by recall antigen-induced in
vitro proliferation and TCR repertoire analysis. These results indicate
that KIR effect on T cells varies upon cell activation stage and show
unexpected complexity in the biological function of KIRs in vivo.
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