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International Immunology, Vol. 15, No. 6, pp. 765-772, June 2003
© 2003 Japanese Society for Immunology

HLA-B*0702 transgenic, H-2KbDb double-knockout mice: phenotypical and functional characterization in response to influenza virus

Pierre-Simon Rohrlich1,2, Sylvain Cardinaud2, Hüseyin Firat3, Mustapha Lamari4, Pascale Briand5, Nicolas Escriou6 and François A. Lemonnier2

1 Hôpital Robert Debré, 48 Bd Serurier, 75019 Paris, France 2 Unité d‘Immunité Cellulaire Antivirale, Département d‘Immunologie, Institut Pasteur, 28 rue du Dr Roux, 75724 Paris Cedex 15, France 3 Généthon III, CNRS URA 1922, 1 rue de l’Internationale, 91002 Evry Cedex, France 4 Hôpital Robert Debré, Etablissement Français du Sang, 48 Bd Serurier, 75019 Paris, France 5 Unité de Physiopathologie Infectieuse et Tumorale des Epithelia, Institut Cochin de Génétique Moléculaire, 24 rue du Fbg Saint-Jacques, 75014 Paris Cedex 18, France 6 Unité de Génétique Moléculaire des Virus Respiratoires, Département de Virologie, Institut Pasteur, 27 rue du Dr Roux, 75724 Paris Cedex 15, France

The first two authors contributed equally to the work
Correspondence to: F. Lemonnier; E-mail: flemonn{at}pasteur.fr
Transmitting editor: H. Ploegh

HLA-B*0702 transgenic mice (expressing a chimeric heavy chain with a murine {alpha}3 domain: HLA-B7m{alpha}3) in which the H-2Kb and H-2Db class I-a (Cl I-a–/–) genes have been inactivated were compared with H-2KbDb Cl I-a+/+ positive controls. Expression of the HLA-B7m{alpha}3 molecules resulted in a 3- to 4-fold increase in peripheral CD8+ T lymphocyte numbers compared to H-2 Cl I-a–/– knockout mice. These cells show a diversified TCR repertoire. Following influenza infection, a significant improvement in HLA-B0702-restricted cytotoxic T lymphocyte (CTL) responses was observed in HLA-B7m{alpha}3, H-2 Cl I-a–/– compared to HLA-B7m{alpha}3, H-2 Cl I-a+/+ mice. The CTL response of infected HLA-B7m{alpha}3, H-2 Cl I-a–/– mice was directed against the nucleoprotein (NP) 418–426 epitope in which mutations have accumulated. Whereas all NP 418–426 variant peptides induced a CTL response, cross-reactivity to the variants was affected. These NP mutations could have been selected over time in humans for the virus to escape HLA-B0702-restricted CTL responses since a similar response was seen in humans with, as in mice, altered cross-recognition of the NP 418–426 variants. These animals may prove a suitable model to study HLA-B0702-restricted CTL responses.

Keywords: cytotoxic T lymphocyte


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