Evidence map›Paper›PMID 42004951›Full record

ReviewFrontiers in immunology2026

JAK inhibition in PD-1 immunotherapy and tumor microenvironment.

Ziyuan Liu, Jiaqi Liu, Hongyu Chu, Zhuming Lu, Shengshan Xu, Yanguo Qin, Lianfang Zhao, Chi Zhang

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed.

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  3. Radiation-induced CD200Cellular & molecular immunology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Ziyuan LiuDepartment of Orthopedics, The Second Hospital of Jilin University, Changchun, Jilin, China.
Jiaqi LiuGuangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
Hongyu ChuDepartment of Gastrointestinal, Colorectal and Anal Surgery, China-Japan Union Hospital of Jilin University, Changchun, China.
Zhuming LuDepartment of Thoracic Surgery, Jiangmen Central Hospital, Jiangmen, Guangdong, China.
Shengshan XuDepartment of Thoracic Surgery, Jiangmen Central Hospital, Jiangmen, Guangdong, China.
Yanguo QinDepartment of Orthopedics, The Second Hospital of Jilin University, Changchun, Jilin, China.
Lianfang ZhaoDepartment of Medical Genetics, Suining Central Hospital, Suining, Sichuan, China.
Chi ZhangGuangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeting the programmed cell death 1 (PD-1)/PD-L1 axis has revolutionized cancer therapy; however, the durability of clinical responses is frequently compromised by chronic inflammation and an immunosuppressive tumor microenvironment (TME). The Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway serves as a central intracellular node integrating cytokine signals that drive these resistance mechanisms. While physiological JAK/STAT signaling is essential for antitumor immunity, its persistent aberrant activation promotes malignant progression, upregulates PD-L1 expression, and orchestrates an immunosuppressive landscape by recruiting myeloid-derived suppressor cells (MDSCs) and polarizing tumor-associated macrophages (TAMs) toward an M2 phenotype, ultimately leading to T cell exhaustion. This review comprehensively elucidates the multifaceted role of JAK/STAT signaling in shaping the immune architecture of both hematologic and solid tumors. We examine the molecular crosstalk between JAK/STAT activation and key immune subsets within the TME and discuss the rationale for repurposing JAK inhibitors-established agents for autoimmune disorders-as adjuvants to immunotherapy. Emerging preclinical and clinical evidence suggests that combining selective JAK inhibition with PD-1 blockade can disrupt inflammatory feedback loops, reprogram the TME, and overcome resistance to immune checkpoint inhibitors. This synergistic strategy represents a promising therapeutic frontier for improving outcomes in refractory malignancies.

Indexed as

Immune Checkpoint InhibitorsImmunotherapyJanus Kinase InhibitorsJanus KinasesNeoplasmsProgrammed Cell Death 1 ReceptorTumor MicroenvironmentAnimalsHumansSignal TransductionSTAT Transcription FactorsT-Cell ExhaustionImmune Checkpoint InhibitorsJanus Kinase InhibitorsJanus KinasesPDCD1 protein, humanProgrammed Cell Death 1 ReceptorSTAT Transcription Factorsimmune checkpoint inhibitorsimmunosuppressionimmunotherapy resistanceJAK/STAT signaling pathwaytumor microenvironment

Identifiers

PMID42004951
PMCPMC13083078

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Registered trials

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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.