ReviewOncoimmunology2026
IL-15 trans-presentation at the innate-adaptive interface: mechanisms and translation in cancer immunotherapy.
Review in Oncoimmunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Durable antitumor immunity requires innate activation, antigen presentation, lymphocyte priming, trafficking, and effector function. In immunologically cold tumors, deficient dendritic-cell and natural killer (NK)-cell activation limits the transition from tumor-antigen recognition to CD8 T-cell immunity. Interleukin-15 (IL-15) is a member of the common gamma-chain cytokine family with a distinctive receptor-delivery system at this innate-adaptive interface. In native trans-presentation, IL-15 is stabilized by IL-15 receptor alpha (IL-15Rα) on an antigen-presenting cell and presented to CD122/CD132 on an apposed NK or memory CD8 T cell. This contact-dependent arrangement supports NK-cell homeostasis, memory CD8 T-cell maintenance, and spatially restricted signaling while avoiding the CD25-dependent regulatory T-cell preference of IL-2. IL-12, IL-15, and IL-18 can generate cytokine-induced memory-like NK cells with enhanced recall. These programs are constrained by intrinsic CISH feedback and by tumor-associated TGF-
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