In current study, we conducted a lentivirus-based overexpression system and observed that overexpressing Tgfb1 successfully promoted the viability and altered the cell cycle distribution in DC. What’s more, this gene also greatly inhibited apoptosis of DC, highlighting the robust immune support effects of Tgfb1 function. Additionally, a quantitative proteomic was implemented to explore the underlying mechanism. Comparing Tgfb1 overexpressed (OE) and normal control (NC) groups, numerous differentially expressed proteins (DEPs) were emerged, which contributed to this phenomenon. Finally, bioinformatics analysis revealed multiple DEPs enriched in immune-related pathways directly or in a roundabout way, which manifested the crucial role played by Tgfb1 in DC.