Abstract:
:The surface density of the triggering receptors responsible for the natural killer (NK)-mediated cytotoxicity is crucial for the ability of NK cells to kill susceptible target cells. In this study, we show that transforming growth factor beta1 (TGFbeta1) down-regulates the surface expression of NKp30 and in part of NKG2D but not that of other triggering receptors such as NKp46. The TGFbeta1-mediated inhibition of NKp30 surface expression reflects gene regulation at the transcriptional level. NKp30 has been shown to represent the major receptor involved in the NK-mediated killing of dendritic cells. Accordingly, the TGFbeta1-dependent down-regulation of NKp30 expression profoundly inhibited the NK-mediated killing of dendritic cells. On the contrary, killing of different NK-susceptible tumor cell lines was variably affected, reflecting the differential usage of NKp30 and/or NKG2D in the lysis of such tumors. Our present data suggest a possible mechanism by which TGFbeta1-producing dendritic cells may acquire resistance to the NK-mediated attack.
journal_name
Proc Natl Acad Sci U S Aauthors
Castriconi R,Cantoni C,Della Chiesa M,Vitale M,Marcenaro E,Conte R,Biassoni R,Bottino C,Moretta L,Moretta Adoi
10.1073/pnas.0730640100keywords:
subject
Has Abstractpub_date
2003-04-01 00:00:00pages
4120-5issue
7eissn
0027-8424issn
1091-6490pii
0730640100journal_volume
100pub_type
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