IL-10 directly suppresses CD4 but not CD8 T cell effector and memory responses following acute viral infection
IL-10 directly suppresses CD4 but not CD8 T cell effector and memory responses following acute viral infection
Mounting effective T cell responses is critical for eliciting long-lasting immunity following viral infection and vaccination. A multitude of inhibitory and stimulatory factors are induced following infection, and it is the compilation of these signals that quantitatively and qualitatively program the ensuing effector and memory T cell response. In response to lymphocytic choriomeningitis virus (LCMV) infection, the immunosuppressive cytokine IL-10 is rapidly up-regulated; however, how IL-10 is regulating what is often considered an “optimal” immune response is unclear. We demonstrate that IL-10 directly inhibits effector and memory CD4 T cell responses following an acutely resolved viral infection. Blockade of IL-10 enhanced the magnitude and the functional capacity of effector CD4 T cells that translated into increased and more effective memory responses. On the other hand, lack of IL-10 signaling did not impact memory CD8 T cell development. We propose that blockade of IL-10 may be an effective adjuvant to specifically enhance CD4 T cell immunity and protection following vaccination.
- University of California, Los Angeles United States
- Scripps Research Institute United States
CD4-Positive T-Lymphocytes, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Statistics, Nonparametric, Interleukin-10, Mice, Inbred C57BL, Mice, Gene Expression Regulation, Animals, Arenaviridae Infections, Cytokines, Lymphocytic choriomeningitis virus, Immunologic Memory
CD4-Positive T-Lymphocytes, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Statistics, Nonparametric, Interleukin-10, Mice, Inbred C57BL, Mice, Gene Expression Regulation, Animals, Arenaviridae Infections, Cytokines, Lymphocytic choriomeningitis virus, Immunologic Memory
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