Abstract:
:HPV-16 is the major causes of cervical cancer. Persistence of infection is a necessary event for progression of the infection to cancer. Among other factors, virus persistence is due the viral proteins fighting the immune response. HPV-16 E5 down-regulates MHC/HLA class I, which is much reduced on the cell surface and accumulates in the Golgi apparatus in cells expressing E5. This effect is observed also in W12 cells, which mimic early cervical intraepithelial progression to cervical cancer. The functional effect of MHC I down-regulation on human CD8 T cells is not known, because of the need for HLA-matched, HPV-specific T cells that recognise E5 expressing-cells. Here we employ a heterologous cell/MHC I system which uses mouse cells expressing both E5 and HLA-A2, and A2-restricted CTLs; we show that the E5-induced reduction of HLA-A2 has a functional impact by reducing recognition of E5 expressing cells by HPV specific CD8+ T cells.
journal_name
Virologyjournal_title
Virologyauthors
Campo MS,Graham SV,Cortese MS,Ashrafi GH,Araibi EH,Dornan ES,Miners K,Nunes C,Man Sdoi
10.1016/j.virol.2010.07.044subject
Has Abstractpub_date
2010-11-10 00:00:00pages
137-42issue
1eissn
0042-6822issn
1096-0341pii
S0042-6822(10)00502-7journal_volume
407pub_type
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