ArticleOncoimmunology2015
Interferon-γ-induced activation of JAK1 and JAK2 suppresses tumor cell susceptibility to NK cells through upregulation of PD-L1 expression.
Article in Oncoimmunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 212 papers.
What it found
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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.
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Who cites it
212 citing papers in PubMed, 306 citations in OpenAlex.
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- Safety and activity of pembrolizumab in combination with rituximab in relapsed or refractory follicular lymphoma.Blood advances · 2022Trial
- IFN-γ-related mRNA profile predicts clinical response to PD-1 blockade.The Journal of clinical investigation · 2017Trial
- Metabolic immune checkpoints (MICs) in cancer: from molecular mechanisms to challenges and opportunities in clinical translation.Signal transduction and targeted therapy · 2026Review
- Reprogramming resistance in advanced lung cancer: epigenetic modulation to restore therapeutic vulnerability.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Coordinated post-transcriptional regulation facilitates PD-L1 protein production and tumor immune suppression.Cancer letters · 2026Article
- Combination Immunotherapy as a Promising Strategy to Overcome Immunotherapy Resistance: From Emergence to Next-Generation Approaches.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Signal Transduction and Transcription Activator 1 in Pan-Cancer: Prognostic and Immunological Value.Clinical and experimental medicine · 2026Article
- Natural and Engineered Cytokines as Cancer Therapeutics.Annual review of cancer biology · 2026Article
- G3BP2-K76 acetylation promotes tumor immunoescape by stabilizing PD-L1 expression in colorectal cancer.Cell communication and signaling : CCS · 2026Article
- Interferon-gamma-inducible protein 30 prevents IFN-γ-receptor 1 degradation to maintain PD-L1 and MHC-II levels in metastatic melanoma.Cell communication and signaling : CCS · 2026Article
- Increased Expression of HLA-DR and CD69 on Peripheral CD4ImmunoTargets and therapy · 2026Article
- Prognostic and Immunological Value of CTNNB1 in Pancreatic Adenocarcinoma: A Comprehensive NGS and Multicomponent Analysis.Genetics research · 2026Article
- Vemurafenib, cetuximab and camrelizumab in BRAF V600E-mutated/MSS metastatic colorectal cancer.Journal of translational medicine · 2025Article
- Article
- Epigenetic Treatment Alters Immune-Related Gene Signatures to Increase the Sensitivity of Anti PD-L1 Drugs.Cancers · 2025Article
- Review
- Masters of adaptation: How cancer and immune cell plasticity mediates tumor progression.PLoS biology · 2025Review
- Threading the Needle: Navigating Novel Immunotherapeutics in Pancreatic Ductal Adenocarcinoma.Cancers · 2025Review
152 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Inhibition of JAK1 or JAK2 in human tumor cells was previously shown to increase susceptibility of these cells to NK cell lysis. In the present study, we examined the cellular mechanisms that mediate this effect in hematopoietic tumor cell lines and primary tumor cells. Incubation of tumor cells with supernatant from activated NK cells or interferon-gamma (IFNγ)-induced activation of pSTAT1 and increased expression of PD-L1 without altering expression of other activating or inhibitory NK cell ligands. These functional effects were blocked by chemical JAK inhibition or shRNAs targeting JAK1, JAK2 or STAT1. Inhibition of IFNγ signaling also prevented the upregulation of PD-L1 and blocking PD-L1 resulted in increased tumor lysis by NK cells. These results show that NK cell activation and secretion of IFNγ results in activation of JAK1, JAK2 and STAT1 in tumor cells, resulting in rapid up-regulation of PD-L1 expression. Increased expression of PD-L1 results in increased resistance to NK cell lysis. Blockade of JAK pathway activation prevents increased PD-L1 expression resulting in increased susceptibility of tumor cells to NK cell activity. These observations suggest that JAK pathway inhibitors as well as PD-1 and PD-L1 antibodies may work synergistically with other immune therapies by preventing IFN-induced inhibition of NK cell-mediated tumor cell lysis.
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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.