Receptor-interacting protein kinase 3 (RIPK3) is one of the key components of necrotic complex, which mediates the development of programmed cell necrosis. Our previous studies have revealed that the initial response of total influenza antigen-specific CD8^＋T cells is partially dependent on RIPK3, but its role in memory CD8^＋T cell response is unclear yet. In this study, we observed that the frequency of influenza specific CD8^＋T cells and their ability to secrete cytokine IFN-γ and TNF-α in RIPK3 knockout mice were significantly lower than those in wild-type mice 37 days after the initial infection of H1N1 A/Puerto Rico/8/34 strain (PR8) in C57BL/6 mice. After the re-challenging infection of H1N1virus PR8, the frequency of viral specific CD8^＋T cells and their ability to secrete cytokine IFN-γ in RIPK3 knockout mice were still significantly lower than those in wild-type mice. In addition, while the frequency of CD8^＋central memory T cells (TCM) in RIPK3 knockout mice was significantly higher than that in wild-type mice, the proportion of effective memory T cells (TEM) or effective T cells (TEff) was significantly lower than that in wild-type mice. These results indicate that RIPK3 is involved in the regulation of the number and secretion of cytokines of influenza virus specific memory CD8^＋T cells, and affects the ratio of TCM to TEM or TEff in memory CD8^＋T cells, which provide new clues for further exploring the molecular mechanism of virus specific memory CD8^＋T cell response.