ArticleImmunotherapy advances2025
Cytokine-induced memory-like NK cells combined with Tafasitamab demonstrate efficacy against B-cell acute lymphoblastic leukemia.
Article in Immunotherapy advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06643221 (Exercise-induced Adrenergic Receptor Signaling as an Immune Adjuvant for Allogeneic Cell Therapies), which is not on this map. Cited by 2 papers.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Exercise-induced Adrenergic Receptor Signaling as an Immune Adjuvant for Allogeneic Cell Therapies
Who cites it
2 citing papers in PubMed.
- Blinatumomab bypasses CD28 blockade to sustain T-cell cytotoxicity and improve survival in a xenograft B-ALL model.Journal for immunotherapy of cancer · 2026Article
- Exercise-mobilized lymphocytes enhance the function of cytokine-induced memory-like NK cells against myeloid leukemia.Blood advances · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
Cytokine-induced memory-like natural killer cells (CIMLNK) represent a novel form of adoptive cellular therapy that is easy to manufacture and readily available. These cells are generated after overnight stimulation of purified natural killer (NK) cells with interleukin-12 (IL-12), interleukin-15 (IL-15), and interleukin-18 (IL-18). While CIMLNK has demonstrated efficacy in patients with relapsed or refractory acute myeloid leukemia (AML), its potential application in B-cell acute lymphoblastic leukemia (B-ALL) remains unclear. Tafasitamab (TAFA), a monoclonal antibody (mAb) directed against CD19, a surface antigen expressed on B-ALL cells, has been developed to augment anti-tumor efficacy through antibody-dependent cellular cytotoxicity (ADCC), a mechanism predominantly mediated by NK cells. Consequently, we sought to assess the susceptibility of B-ALL to the combination of CIMLNK and TAFA using three B-ALL cell lines: NALM6, SUP-B15, and RS4;11. The addition of TAFA significantly augmented the cytotoxic activity, degranulation capacity, and IFN-γ production of CIMLNK. TAFA-induced ADCC was found to be dose-dependent and was abolished after CD16 blockade. Furthermore, TAFA-mediated effects against NALM6 and SUP-B15 were more pronounced in CIMLNK compared to unstimulated NK cells. In vivo, the combination of CIMLNK and TAFA led to a more pronounced survival benefit in leukemia-bearing mice. In summary, our findings suggest that this combination holds promise as a potential alternative treatment option for patients with relapsed refractory B-ALL.
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