Shutdown of an acute T cell immune response to viral infection is mediated by the proapoptotic Bcl-2 homology 3-only protein Bim
Copyright policy )Shutdown of an acute T cell immune response to viral infection is mediated by the proapoptotic Bcl-2 homology 3-only protein Bim
We used mutant Fas-deficient (lpr) or Bim-deficient mice to investigate the role of the death receptor and Bcl-2-regulated apoptotic pathways in terminating a physiological T cell response to herpes simplex virus infection. In WT andlprmice CD8+antigen-specific T cells were deleted after viral clearance. In contrast, the immune response was not terminated in Bim-deficient mice despite viral clearance, and CD8+antigen-specific T cells accumulated in the spleen. Thus, Bim is dispensable for viral clearance but is necessary for the death of activated T cells when immune responses are terminated. These findings have implications for the therapeutic manipulation of immune responses to infections and immunization.
- University of Queensland Australia
- Walter and Eliza Hall Institute of Medical Research Australia
- University of Queensland Australia
Male, Mice, Knockout, Mice, Inbred MRL lpr, Bcl-2-Like Protein 11, Interleukin-7, Membrane Proteins, Apoptosis, Herpes Simplex, Herpesvirus 1, Human, CD8-Positive T-Lymphocytes, Lymphocyte Activation, Mice, Inbred C57BL, Kinetics, Mice, 1000 General, Animals, Female, Lymph Nodes, Apoptosis Regulatory Proteins, Carrier Proteins, Cell Division
Male, Mice, Knockout, Mice, Inbred MRL lpr, Bcl-2-Like Protein 11, Interleukin-7, Membrane Proteins, Apoptosis, Herpes Simplex, Herpesvirus 1, Human, CD8-Positive T-Lymphocytes, Lymphocyte Activation, Mice, Inbred C57BL, Kinetics, Mice, 1000 General, Animals, Female, Lymph Nodes, Apoptosis Regulatory Proteins, Carrier Proteins, Cell Division
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