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The Journal of Immunology, 1979, 122: 2611-2616.
Copyright © 1979 by The American Association of Immunologists, Inc.

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Natural Killing of Measles-Infected Cells by Human Lymphocytes1

Kenneth A. Ault and Howard L. Weiner2

From the Departments of Pathology and Microbiology, Harvard Medical School and the Department of Medicine and Section of Neurology, Peter Bent Brigham Hospital, Boston, Massachusetts 02115

Abstract

HeLa cells persistently infected with measles virus (M-HeLa) show markedly increased susceptibility to natural killing (NK) by normal human blood lymphocytes compared to uninfected HeLa cells. The killing is mediated by the same population of non-B, non-T lymphocytes with avid Fc receptors for IgG that mediate other forms of NK and antibody-dependent cellular cytotoxicity (ADCC). There is no evidence that this NK is mediated by antibody; specifically, the killing regenerates after being abolished by extensive treatment of the effector cells with trypsin or pronase, and it cannot be inhibited by large amounts of F(ab')2 fragments of anti-measles antibody or by a large excess of normal {gamma}-globulins. In addition, NK of M-HeLa is strongly correlated (r = 0.79, p < 0.001) with NK of an unrelated cell line (K-562) that does not contain measles virus and is a standard target for NK. The strong correlation between NK of M-HeLa and K-562 is confirmed by cold-target inhibition studies showing cross-competition between the two cell lines. Killing cannot be enhanced by addition of supernatants from lymphocytes cultured with M-HeLa to fresh lymphocytes cultured with M-HeLa, HeLa, K-562, or other cell lines, making it unlikely that interferon or other soluble factors have a role in this system. These studies suggest that persistent infection of HeLa cells with measles virus results in the modification of the HeLa cell membrane and that this modification is similar to some structure on K-562 that is important for NK. In addition, these studies raise the possibility that NK could play a role in host defenses against measles virus infection.

Footnotes

1 This work was supported by National Cancer Institute Grants CA 14723 and CA 22109 and by National Multiple Sclerosis Society Grant RC991-A-3.

2 Howard L. Weiner is the recipient of a Teacher-Investigator Award from the National Institute of Neurological and Communicative Disorders and Strokes, No. NSI-EA1K07 NS 237-1 NSPB.







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