Abstract: Objective To study the effect of T cell killing ability on low-dose decitabine (DAC) treated cervical cancer cells and explore its possible mechanism. Methods CCK-8 was used to test the proliferation of low-dose DAC treated cervical cancer cells. Flow cytometry assay was used to test the apoptosis and cell cycle of low-dose DAC treated cervical cancer cells. CCK-8 was also used to test T cell killing ability of low-dose DAC treated cervical cancer cells. Real-Time PCR was used to test the expression of BORIS, NYESO-1, MAGEA1, MAGEA3, MAGEA4 and FasL on low-dose DAC treated cervical cancer cells. Results 10 nmol/L of DAC showed no significant difference in the proliferation and apoptosis of cervical cancer cells, while 100 nmol/L of DAC inhibited the proliferation of cervical cancer cells. Though 10 nmol/L of DAC did not inhibit the proliferation of cervical cancer cells directly, it enhanced T cell killing ability to cervical cancer cells most significantly with the efficient targeting ratio of 10:1. Also 10 nmol/L of DAC showed significant up-regulation in the mRNA expression of CTAs such as BORIS, NYESO-1, MAGEA1, MAGEA3 and MAGEA4, as well as FasL. Conclusion These results suggest that low-dose DAC may work as a potential biological immunotherapy drug to inhibit cell viability and enhance T cell killing ability in cervical cancer cells.