It has been shown that silencing of suppressor of cytokine signalling 1 (Socs1) 
or stably expressing transgenic protein Ags in antigen-presenting dentritic 
cells (DCs) strongly enhances antigen-specific anti-tumour immunity. However, 
whether the strong and long-lasting T cell responses induced by the modified DCs 
could modulate the immunosuppressive tumour microenvironment has not been 
clarified. In this study, we explored the anti-tumour immunity of DCs modified 
by Socs1-shRNA lentiviral transduction combined with sustained expression of 
TRP2 in different tumour models. We showed that transfer Socs1-silenced or 
tumour antigen TRP2 persistent expressed DCs, or DCs modified by combination of 
Socs1-silencing and sustaining TRP2 expression prior to inoculation of tumour 
cells delayed B16 tumour cell growth, prolonged mouse survival and increased the 
ratio of CD8+ T/Treg as well as the CTL activity in tumours. However, there was 
no significant effect on tumour growth and mouse survival rate upon tumour 
established. Further, we showed that tumour cell secreted IL-10 counteracted the 
immunity of modified DCs in established tumour model, injection of Socs1-shRNA 
and TRP2 antigen modified significantly inhibited growth of the established 
B16-IL-10(-/-) tumours. These data indicated that the high level of IL-10 within 
tumour microenvironment is one of factors that compromise DC vaccine functions.