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. 1980 Oct;42(1):136–143.

Cellular cytotoxicity to measles virus during natural measles infection

H C Whittle, J Werblinska
PMCID: PMC1537059  PMID: 7460389

Abstract

Little is known about cellular cytotoxicity to measles virus during natural measles infection which is still a major cause of death in many parts of the world. Therefore we measured the ability of peripheral blood mononuclear cells (PBM) from children with measles to kill Hela cells persistently infected with measles virus. In a 6-hr 51CR-release assay antibody-independent cellular cytotoxicity was shown to be low during the acute stage of measles. This rose to a maximum 1 week after the onset of the rash and fell rapidly on recovery 2 to 3 weeks later. The respective means values for the three periods (expressed as specific immune release of 51Cr) were 7·9±8·4%, 31·0±16·4% and 6·1±7·7%. Killing in this assay was not effected by T lymphocytes, for concentration of these cells by three different methods failed to increase cytotoxic power. In contrast peripheral blood mononuclear cells depleted of T lymphocytes showed greatly increased antibody-independent cellular cytotoxicity. Antibody-dependent cellular cytotoxicity was not found to vary significantly with the stage of measles. The mean values were 30·0±13·6%, 26·6±11·7% and 23·9±12·1% for the periods 0–2, 3–14 and 15–30 days after the onset of the rash. Both antibody-independent and antibody-dependent cellular cytotoxicity of PBM were lowered by layering these cells on immune complexes fixed to plastic or by incubating them with normal rabbit γ-globulin. Antibody-dependent cellular cytotoxicity was also lowered in the presence of 10% acute-phase autologous plasma. We concluded that antibody-independent cytoxocity was effected either by natural killer cells or by K cells using traces of antibody present in the assay. Antibody-dependent cellular cytotoxicity which is due to K cells may be modulated by circulating immune complexes during the course of disease.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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