Objective To investigate whether RIP3 (receptor-interacting protein 3) is involved in the inductionof influenza antigen specific CD8⁺ T cell responses in C57BL/6 mice upon H1N1 influenza virus infection. Methods RIP3knockout (RIP3^{-/ -} ) and wild type (WT) C57BL/6 mice were infected by influenza virus H1N1 PR8 with the dose of 0. 7×10³ TCID₅₀(50% tissue culture infective dose). Splenocytes were isolated from the infected mice which were sacrificed at 8days post infection (d.p.i), and fluorescence-activated cell sorting (FACS) were used for the comparison of quantities andfunctions of influenza viral antigen specific CD8⁺ T cells between the RIP3^{-/ -} group and WT group. Surface staining ofinfluenza viral MHC I tetramer was performed to quantify the antigen specific CD8⁺ T cells. Intracellular cytokine staining(ICS) was carried out to dissect the production levels of effector cytokines, such as IFN-γ, TNF-α and IL-2. Granzyme B,which is related to the cytotoxic effect of the antigen specific CD8⁺ T cells, was also assayed by ICS. Results On average,the percentages of influenza viral antigen specific CD8⁺ T cells in the WT group of mice were about 2. 71 fold comparingwith that in the RIP3^{-/ -} group of mice. Furthermore, the production levels of IFN-γ, TNF-α and IL-2 by the antigen specificCD8⁺ T cells in the WT group of mice were significantly higher than those levels in the counterpart group of RIP3^{-/ -} mice( P < 0. 01); and in regards to granzyme B, the same trend was showed when comparing the expression levels between thosetwo group mice, i.e., WT group was higher than the RIP3^{-/ -} group ( P < 0. 01). Conclusions The data of the presentstudy reported that the deficiency of RIP3 molecule in C57BL/6 mice will decrease the quantity and functionality of theinfluenza viral antigen specific CD8⁺ T cells at 8 d.p.i. upon influenza virus H1N1 PR8 infection, which indicates that RIP3 is indispensable for the induction of influenza viral antigen specific CD8⁺ T cells at effector stage.