Natural killer (NK) cells destroy virus-infected and tumour cells, apparently without the need for previous antigen stimulation. In part, target cells are recognized by their diminished expression of major histocompatibility complex (MHC) class I molecules, which normally interact with inhibitory receptors on the NK cell surface. NK cells also express triggering receptors that are specific for non-MHC ligands; but the nature of the ligands recognized on target cells is undefined. NKp46 is thought to be the main activating receptor for human NK cells. Here we show that a soluble NKp46-immunoglobulin fusion protein binds to both the haemagglutinin of influenza virus and the haemagglutinin-neuraminidase of parainfluenza virus. In a substantial subset of NK cells, recognition by NKp46 is required to lyse cells expressing the corresponding viral glycoproteins. The binding requires the sialylation of NKp46 oligosaccharides, which is consistent with the known sialic binding capacity of the viral glycoproteins. These findings indicate how NKp46-expressing NK cells may recognize target cells infected by influenza or parainfluenza without the decreased expression of target-cell MHC class I protein.
A consideration of the list brings out one or two interesting points. The commonest fungus is Arthrobotrya oligospora (21 records), which is not surprising in view of its widespread distribution in many kinds of habitat1. Its great preponderance over all other species except 'Mycelium 186' is, however, surprising. Easily the second commonest is 'Mycelium 186' (18 records); as this fungus has been recorded only from soil, it would seem likely that it is a specialized soil species, and it is possible that its constant failure to produce spores when grown on a.gar media may be correlated with this. How it reproduces in its natural habitat is not known, but among other factors the disruption of soil by earthwonns might perhaps be considered. Like Arthrobotrys oligospora, it outnumbers other fungi in the list to a surprising extent. Arthrobotrys dactyloides, capturing eelworms by means of constricting rings, appears to be more frequent in soil than elsewhere. It has been obtained in Great Britain from compost by Dixon (personal communication), but apart from its occurrence in soil it does not appear to be a common British species. It has also been observed in Danish soil by Shepherd (in litt.). Trichothecium cystosporium is fairly prominent, and this species has also been isolated from soil on a previous occasion•. The other species in the list call for no particular comment, though the frequencies of the ubiquitous Harpoaporium anguillulae and Acroatalagmus obovatus may be noted. The preponderance of hyphomycetes capturing nematodes by means of adhesive networks is also interesting.Attempts to correlate the presence or absence of particular fungi with soil factors such as pH, etc., yielded no results ; but it is clear that many more soil samples will have to be examined before any such correlations, if present, can be expected to become apparent. Quantitative information on the distribution of predacious fungi in soil is also badly needed ; this work is now in hand, and it is hoped to make it the subject of a future communication.I should like to express my thanks to Mr. F. G. W. Jones, School of Agriculture, Cambridge; to Mr.
Treatment of human T-cell leukemia virus type I (HTLV-I)and HTLV-II-infected T-cell lines with 12-0-tetradecanoylphorbol-13-acetate (TPA) stimulated virus release. However, this stimulation was mainly detected at 42 to 48 h of treatment, whereas later virus release declined rapidly. During the first 48 h, TPA had no effect on cell growth, but later, the number of viable cells was profoundly lower in the TPA-treated than in the untreated cultures. This shift in virus release and cell number resulted from self-fusion of a large proportion of the virus-producing cells, which seemed to consequently enter into a dying process. This fusion, which resulted in syncytium formation, was strongly inhibited by anti-HTLV-I env monoclonal antibodies. Furthermore, no self-fusion was detected in three different uninfected T-cell lines similarly treated with TPA. On the other hand, stimulation of virus production by 3-methylcolanthrene (3-MC) treatment failed to induce self-fusion in the infected cells. Moreover, no syncytium was detected when these 3-MC-treated infected cells were cocultured with any of the TPA-treated uninfected cells. The effects of TPA on virus production and syncytium formation were both abolished by three different protein kinase C inhibitors. Taken together, these data suggest that the self-fusion observed in these experiments required both enhanced virus production and protein kinase C-phosphorylated viral or/and virally induced cellular component(s).
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