Until now, it has been unclear whether murine cytomegalovirus (MCMV)-encoded protein m144 directly regulates natural killer (NK) cell effector function and whether the effects of m144 are only strictly evident in the context of MCMV infection. We have generated clones of the transporter associated with antigen processing (TAP)-2–deficient RMA-S T lymphoma cell line and its parent cell line, RMA, that stably express significant and equivalent levels of m144. In vivo NK cell–mediated rejection of RMA-S-m144 lymphomas was reduced compared with rejection of parental or mock-transfected RMA-S clones, indicating the ability of m144 to regulate NK cell–mediated responses in vivo. Significantly, the accumulation of NK cells in the peritoneum was reduced in mice challenged with RMA-S-m144, as was the lytic activity of NK cells recovered from the peritoneum. Expression of m144 on RMA-S cells also conferred resistance to cytotoxicity mediated in vitro by interleukin 2–activated adherent spleen NK cells. In summary, the data demonstrate that m144 confers some protection from NK cell effector function mediated in the absence of target cell class I expression, but that in vivo the major effect of m144 is to regulate NK cell accumulation and activation at the site of immune challenge.
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2 August 1999
Article|
August 02 1999
M144, a Murine Cytomegalovirus (Mcmv)-Encoded Major Histocompatibility Complex Class I Homologue, Confers Tumor Resistance to Natural Killer Cell–Mediated Rejection
Erika Cretney,
Erika Cretney
aFrom the Cellular Immunity Laboratory, The Austin Research Institute, Melbourne 3084, Victoria, Australia
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Mariapia A. Degli-Esposti,
Mariapia A. Degli-Esposti
bDepartment of Microbiology, The University of Western Australia, Perth 6009, Western Australia, Australia
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Eloise H. Densley,
Eloise H. Densley
bDepartment of Microbiology, The University of Western Australia, Perth 6009, Western Australia, Australia
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Helen E. Farrell,
Helen E. Farrell
cCentre for Preventative Medicine, Suffolk CB8 7UU, United Kingdom
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Nick J. Davis-Poynter,
Nick J. Davis-Poynter
cCentre for Preventative Medicine, Suffolk CB8 7UU, United Kingdom
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Mark J. Smyth
Mark J. Smyth
aFrom the Cellular Immunity Laboratory, The Austin Research Institute, Melbourne 3084, Victoria, Australia
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Erika Cretney
aFrom the Cellular Immunity Laboratory, The Austin Research Institute, Melbourne 3084, Victoria, Australia
Mariapia A. Degli-Esposti
bDepartment of Microbiology, The University of Western Australia, Perth 6009, Western Australia, Australia
Eloise H. Densley
bDepartment of Microbiology, The University of Western Australia, Perth 6009, Western Australia, Australia
Helen E. Farrell
cCentre for Preventative Medicine, Suffolk CB8 7UU, United Kingdom
Nick J. Davis-Poynter
cCentre for Preventative Medicine, Suffolk CB8 7UU, United Kingdom
Mark J. Smyth
aFrom the Cellular Immunity Laboratory, The Austin Research Institute, Melbourne 3084, Victoria, Australia
1used in this paper: B6, C57BL/6; HCMV, human CMV; LIR, leukocyte Ig-like receptor; MCMV, murine CMV; P0, perforin-deficient; RAG, recombination activating gene; TAP, transporter associated with antigen processing
Received:
April 26 1999
Revision Requested:
June 02 1999
Accepted:
June 07 1999
Online ISSN: 1540-9538
Print ISSN: 0022-1007
© 1999 The Rockefeller University Press
1999
The Rockefeller University Press
J Exp Med (1999) 190 (3): 435–444.
Article history
Received:
April 26 1999
Revision Requested:
June 02 1999
Accepted:
June 07 1999
Citation
Erika Cretney, Mariapia A. Degli-Esposti, Eloise H. Densley, Helen E. Farrell, Nick J. Davis-Poynter, Mark J. Smyth; M144, a Murine Cytomegalovirus (Mcmv)-Encoded Major Histocompatibility Complex Class I Homologue, Confers Tumor Resistance to Natural Killer Cell–Mediated Rejection. J Exp Med 2 August 1999; 190 (3): 435–444. doi: https://doi.org/10.1084/jem.190.3.435
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