The role of NK1.1+ cells in the protection against MHC class I+ HPV16-associated tumours
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
15709715
PII: file/5970/fb2004a0029.pdf
Knihovny.cz E-zdroje
- MeSH
- buňky NK účinky léků imunologie MeSH
- histokompatibilita - antigeny třídy I analýza genetika MeSH
- infekce papilomavirem genetika imunologie prevence a kontrola MeSH
- lymfocytární deplece MeSH
- myši MeSH
- nádorové buněčné linie MeSH
- onkogenní proteiny virové genetika MeSH
- protilátky farmakologie MeSH
- represorové proteiny genetika MeSH
- transplantace nádorů MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- E6 protein, Human papillomavirus type 16 MeSH Prohlížeč
- histokompatibilita - antigeny třídy I MeSH
- oncogene protein E7, Human papillomavirus type 6 MeSH Prohlížeč
- onkogenní proteiny virové MeSH
- protilátky MeSH
- represorové proteiny MeSH
Depletion of NK1.1+ cells by repeated i.p. injections of PK136 antibody significantly enhanced growth of MHC class I+ tumours in syngeneic mice. Depletion starting before tumour transplantation or on the day of transplantation substantially accelerated tumour growth; depletion starting on day 7 or 14 after tumour transplantation was without any effect. These results indicate that the NK1.1+ cells play an important inhibitory role during the early phase of the growth of some MHC class I+ tumours. Since the relevant target for NK cells is a "missing self" signal, absence of the MHC class I molecules, the NK cells cannot be expected to directly inhibit the growth of the MHC class I+ tumours. The results indicate that the effects of non-NK cells or indirect effects mediated by NK cell interactions and release of cytokines were responsible for the results.