ArticleScientific reports2025
Macrophage-derived pro-inflammatory cytokines augment the cytotoxicity of cytokine-induced killer cells by strengthening the NKG2D pathway in multiple myeloma.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- Targeting the MICA/B-NKG2D axis in cancer: from molecular structure to immunotherapeutic strategies-a narrative review.Translational cancer research · 2026Review
- Targeting PRKCN, an Essential Driver Orchestrating mTOR-IRF4 Axis Independently of Kinase Activity, in Multiple Myeloma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitophagy-driven multidimensional regulation of tumor immune evasion and context-dependent therapeutic strategies.Journal of translational medicine · 2026Review
- Review
- Association Between Amino Acid Polymorphisms in MICA and MICA-NKG2D Interaction Affinity: Implications and Significance for Tumor Immunity.Biomolecules · 2025Review
- PI3K Signaling Pathway Inhibitor Affects Myeloma Cells in a Culture-Dependent Manner.Advanced pharmaceutical bulletin · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple myeloma (MM) is a clonal hematologic malignancy characterized by low rate of complete remissions. Cytokine-induced killer (CIK) cell therapy has shown promising benefits in MM treatment. In this study, we investigated whether the pro-inflammatory cytokines secreted by macrophages could upregulate MICA/B expression and thus the cytotoxicity of CIK cells. Flow cytometry was used for phenotypic measurement and the cytotoxicity assay of CIK cells. Soluble MICA/B and macrophage-derived cytokines were measured using ELISA assay. CCK-8 assay was applied to evaluate cell viabilities. Gene expression levels were investigated using RT-qPCR. The expression of MICA/B and PD-L1 in MM cells was upregulated by pro-inflammatory cytokines. Pro-inflammatory cytokines enhanced the cytotoxicity of CIK cells against MM cells, with TNF-α exhibiting a more potent effect than IL-1β and IL-6 as it strengthened both components of the NKG2D-MICA/B axis. PD-L1 blockade promoted the cytotoxic ability of CIK cells. Mechanistically, IL-1β, IL-6, and TNF-α enhanced the transcription of MICA/B and PD-L1 genes via the PI3K/AKT, JAK/STAT3, and MKK/p38 MAPK pathways. Pro-inflammatory cytokines upregulated the expression of MICA/B and PD-L1, thereby promoting the cytotoxicity of CIK cells against MM by strengthening the NKG2D pathway, while PD-L1 blockade enhanced the cytotoxicity of CIK cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.