动物实验,蛋白激酶-3,甲型流感病毒H1N1 z-bo 2020-09-11 393

　　Objective: To study the role of receptor-interacting protein kinase 3 (RIP3) in the specific CD8 + T cell immune response after influenza A virus H1N1 infection in C57BL/6 mice?

　　Method: The H1N1PR8 influenza virus strain used is RIP3 knockout (RIP3-/-) and wild type by nasal instillation, respectively, half of the tissue culture infection dose (50% tissue culture infection dose, TCID50) of 0.7× 103. (WT) C57BL/6 infected mice? Eight days after infection (post infection, dpi), mouse spleen cells were isolated, and fluorescence activated cell selection (FACS): MHC I epitope was used to detect the number and function of influenza antigen-specific CD8 + T cells. Peptide IV tetramer staining is used to stain influenza-specific CD8 + T cells, and intracellular cytokine staining (ICS) is used to produce IFN-γγTNF-αγIL-2 through CD8 + T cells, and the detected effector cytokine levels are for example . Is the expression of granzyme B related to the killing function of CD8 + T cells?

　　Results: After 0.7×103 TCID50 influenza virus infection, the ratio of influenza antigen-specific CD8 + T cells in wild-type mice was RIP3/2.71 times that of mice; CD8 + T cells in wild-type mice were cytokine IFN-γ ? TNF-α? The ability to secrete IL-2 was significantly higher than that of RIP3-/- mice (P\u003c0.01); and the expression level of CD8 + T granzyme B in WT mice was significantly higher than that of RIP3-/- mice. Is it expensive (P\u003c0.01)?

　　Conclusion: The knockout of RIP3 molecules in mice infected with influenza A virus can cause some CD8 + T infections. This is due to the decrease in cell number and function caused by influenza virus infection. Does RIP3 have influenza antigen specificity indicate that it is involved One of the important molecules for CD8 + T cell induction and function?