ArticleJournal for immunotherapy of cancer2026
Novel NK cell-like phenotype expressing CCR5 and its ligands elicits tumor-specific acquired immunity to carcinomatous peritonitis via host NK-derived IFN-γ.
Article in Journal for immunotherapy of cancer, 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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6 authors.
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Abstract
backgroundNatural killer (NK) cell-based immunotherapies remain largely ineffective against solid tumors and strategies that directly enhance NK cell cytotoxicity often fail to establish durable tumor control. To address this limitation, we developed GAIA-102, a novel NK-like phenotype with enhanced tumor-homing capacity, and its scalable derivative, expanded GAIA-102 (exp_GAIA). Here, we evaluated whether exp_GAIA can engage host immunity to drive durable response.
methodsA syngeneic lethal murine model of carcinomatous peritonitis was used to assess exp_GAIA. Following adoptive transfer of exp_GAIA with recombinant human interleukin-2 (rhIL-2), antitumor efficacy, survival and immune response were evaluated. Mechanistic studies quantified chemokine production and examined CCR5-dependent recruitment and expansion of endogenous NK cells, interferon-γ (IFN-γ) secretion, and activation of tumor-specific CD8
resultsTreatment with exp_GAIA plus rhIL-2 induced complete tumor regression and generated durable, tumor-specific adaptive immune response that required CD8
conclusionsIn combination with rhIL-2, exp_GAIA integrates endogenous NK activity with induction of long-lasting, CD8
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