The Journal of Experimental Medicine
CSHL 2010 Immunology Conference
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© The Rockefeller University Press, 0022-1007/1999/8/435/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 3, August 2, 1999 435-444

Original Article

M144, a Murine Cytomegalovirus (Mcmv)-Encoded Major Histocompatibility Complex Class I Homologue, Confers Tumor Resistance to Natural Killer Cell–Mediated Rejection

Erika Cretneya, Mariapia A. Degli-Espostib, Eloise H. Densleyb, Helen E. Farrellc, Nick J. Davis-Poynterc, and Mark J. Smytha

a From the Cellular Immunity Laboratory, The Austin Research Institute, Melbourne 3084, Victoria, Australia
b Department of Microbiology, The University of Western Australia, Perth 6009, Western Australia, Australia
c Centre for Preventative Medicine, Suffolk CB8 7UU, United Kingdom
Cellular Immunity Laboratory, The Austin Research Institute, Studley Road, Heidelberg 3084, Victoria, Australia.61-3-9287-060061-3-9287-0653

m.smyth{at}ari.unimelb.edu.au

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.

Key Words: mouse • tumor immunity • natural killer cells • cytotoxicity • cytomegalovirus

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

© 1999 The Rockefeller University Press


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