
T cell avidity is critical to viral clearance, but mechanisms of CD8+T cell avidity maturation are poorly understood. Here, we find that IL-15 mediates two mechanisms of avidity maturation. (i) By selection at the population level, IL-15 promotes greater survival of high- compared with low-avidity cytotoxic T lymphocytes (CTLs). High-avidity CTLs express higher levels of IL-15Rα and persist longer by homeostatic proliferation. (ii) At the individual cell level, IL-15 induces higher levels of surface coreceptor CD8αβ, increasing functional avidity. IL-15 during priming selects or induces higher-avidity CTLs. Conversely, high-avidity CTLs are diminished in IL-15Rα knockout mice. These results provide an explanation of CD8+T cell avidity maturation and may contribute to the design of novel vaccines.
Interleukin-15, Mice, Knockout, Mice, Inbred BALB C, Receptors, Interleukin-15, Models, Immunological, Cell Differentiation, Receptors, Interleukin-2, CD8-Positive T-Lymphocytes, Recombinant Proteins, Mice, Animals, Homeostasis, Female, Immunologic Memory, T-Lymphocytes, Cytotoxic
Interleukin-15, Mice, Knockout, Mice, Inbred BALB C, Receptors, Interleukin-15, Models, Immunological, Cell Differentiation, Receptors, Interleukin-2, CD8-Positive T-Lymphocytes, Recombinant Proteins, Mice, Animals, Homeostasis, Female, Immunologic Memory, T-Lymphocytes, Cytotoxic
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| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
| impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 10% |
