Cervical cancer (CC) remains a major health challenge with high mortality rates due to chemoresistance and immune escape. However, the underlying mechanisms remain unclear. We investigated the role of TAB2 in CC using cisplatin-resistant and parental cell lines. Cell proliferation, migration, sphere formation and T cell-mediated killing assays were performed. Western blot and qRT-PCR analysed protein and mRNA expression. NF-κB pathway involvement was examined using the BAY 11-7082 inhibitor. TAB2 expression was significantly elevated in cisplatin-resistant CC cells. TAB2 overexpression promoted chemoresistance and immune escape through NF-κB pathway activation. Conversely, TAB2 knockdown or NF-κB inhibition sensitised resistant cells to cisplatin and enhanced T cell-mediated killing. The resistant phenotype could be rescued by restoring PD-L1 expression. Our findings reveal TAB2 as a critical regulator of both chemoresistance and immune escape in CC through NF-κB pathway activation. This suggests TAB2 as a potential therapeutic target for overcoming treatment resistance in CC.