IL-15 induces CD8+ T cells to acquire functional NK receptors capable of modulating cytotoxicity and cytokine secretion

Common gamma chain (¿c) cytokines differentially potentiate TNFR family signaling in antigen-activated CD8 + T cells

“…Consistent with previous reports about recently-activated CD8 + T cells, the transcriptomic data indicated that the IL-9 receptor, CD129, was not substantially expressed in any of the conditions tested, and that the IL-15 receptor, CD215, was expressed at a significantly lower level than the other γc cytokine receptors. In this study, IL-15 did not induce dramatic changes in any of the assessed parameters, a finding which contrasts with those of several other studies investigating the impact of IL-15 on CD8 + T cells [15][16][17][18][19]. The low expression levels of the IL-15 receptor in this particular CD8 + T cell population may account for the muted effect of IL-15 treatment, relative to the other γc cytokines.…”

“…However, expression of IFN-γ by the CD8 + T cells was broadly, and relatively evenly, up-regulated across the treatment groups, suggesting that the mechanism may involve an altered sensitivity to IFN-γ or an alternative signaling pathway, rather than a direct response to increased concentrations of IFN-γ. Alternatively, several studies have shown that CD8 + T cells can acquire NK-associated markers and MHC-unrestricted cytolytic capabilities via treatment with various cytokines, including IL-7, IL-12, IL-15 and IL-21 [15,55,56,58]. However, the inconsistent phenotypic outcomes reported by these studies, as well as the observations from this study, suggest that the capacity of specific cytokines to induce an NK-like polarization in CD8 + T cells may be largely defined by context and timing.…”

Role of Runt-related Transcription Factor 3 (RUNX3) in Transcription Regulation of Natural Cytotoxicity Receptor 1 (NCR1/NKp46), an Activating Natural Killer (NK) Cell Receptor

“…In fact, surface NKp46 can be forcibly induced in a small proportion of human CD8ϩ T cells (ϳ5%), when these cells are cultured ex vivo for 12 days with IL-15 (47). This suggests that the axis plays an important, although by itself not sufficient, role in the NK program.…”

Resveratrol sensitized leukemia stem cell-like KG-1a cells to cytokine-induced killer cells-mediated cytolysis through NKG2D ligands and TRAIL receptors

“…8,29,30 Therefore, we gained CIKs by adding IL-2 and IL-15 and found that CIKs could secrete more IFNγ, express higher levels of NKG2D and TRAIL on the cell-surface, improve cytolytic levels against K562 cells and KG-1a cells relative to PBMCs cytotoxic capabilities. However, in contrast to K562 cells, glioblastoma, melanoma, T-cell leukemia, as well as pancreatic, breast and colon carcinomas, 46 similarly to our findings that RES not only upregulated the expression of DR5, but also downregulated the expression of DcR1 on the surface of KG-1a cells, as a result to sensitize KG-1a cells to TRAIL-induced growth-inhibition and apoptosis.…”