---
title: "Immune-pressure redistribution as a framework for resistance to PD-1/PD-L1 blockade"
id: "pubmed-42763389"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42763389"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42763389/"
doi: "10.1186/s12943-026-02786-4"
published_at: "2026-09-20T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Immune-pressure redistribution as a framework for resistance to PD-1/PD-L1 blockade
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42763389
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42763389/)
- **DOI:** [10.1186/s12943-026-02786-4](https://doi.org/10.1186%2Fs12943-026-02786-4)
- **Published At:** 2026-09-20T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- PD-1/PD-L1 blockade yields durable tumor control in some patients but **primary, adaptive, and acquired resistance** are common, limiting benefit. - The authors propose **immune-pressure redistribution** as a treatment-oriented framework that complements cancer immunoediting by focusing on where immune pressure is diverted after checkpoint release. - Resistance is organized into three coupled topologies: (1) transfer into **tumor-intrinsic escape** (loss of antigen presentation, interferon-response defects, oncogenic rewiring, lineage plasticity); (2) weakening of the anti-tumor response (defective priming, terminal T-cell differentiation, compensatory checkpoints, metabolic constraints, chronic cytokine signaling); and (3) unloading into non-tumor compartments (stromal, vascular, myeloid, regulatory, microbial, and systemic host factors). - The review integrates clinically validated mechanisms with emerging evidence, highlighting the temporal duality of **interferon-JAK signaling** and the role of **tumor-draining lymph nodes** in sustaining progenitor-exhausted T cells. - The authors note limited clinical translation so far for targets such as **TIGIT**, **IDO1**, **TGF-β**, and **CSF-1R**. - They propose a **biomarker-guided strategy** combining tumor visibility, immune-cell state, spatial architecture, systemic inflammation, and early treatment dynamics to identify the dominant resistance topology. - The framework supports **topology-matched combinations** and **adaptive sequencing** rather than uniform escalation, aiming to restore productive immune pressure while reducing compensatory escape and toxicity. - The review is a synthesis of validated mechanisms and emerging data and is intended to inform therapeutic design and predictive biomarker selection for PD-1/PD-L1 blockade resistance.
## Clinical Analysis & Structured Key Points
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Affiliations Expand ### Affiliations * 1 Department of Radiation Oncology, Cancer Center & Institution of Stress Medicine, West China Hospital, Sichuan University, Chengdu, China. * 2 Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China. * 3 Department of Oncology, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, Zhuzhou, China. * 4 Department of Orthopaedics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China. lizhihong@csu.edu.cn. * 5 Hunan Key Laboratory of Tumor Models and Individualized Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China. lizhihong@csu.edu.cn. * 6 Department of Radiation Oncology, Cancer Center & Institution of Stress Medicine, West China Hospital, Sichuan University, Chengdu, China. zoubingwen81@163.com. * 7 Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China. fengyeqian@csu.edu.cn. # Contributed equally. * PMID: **42763389** * DOI: [ 10.1186/s12943-026-02786-4 ](https://doi.org/10.1186/s12943-026-02786-4) Item in Clipboard Review # Immune-pressure redistribution in resistance to PD-1/PD-L1 blockade: mechanisms, biomarkers, and therapeutic design Xiaodong Wang et al. Mol Cancer. 2026. Show details Display options Display options Format Abstract PubMed PMID Mol Cancer Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Mol+Cancer%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Mol+Cancer%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42763389/) . 2026 Sep 20;25(1):222. doi: 10.1186/s12943-026-02786-4. ### Authors [Xiaodong Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+X&cauthor_id=42763389)[#](https://pubmed.ncbi.nlm.nih.gov/42763389/#short-view-equal-contrib-explanation "Contributed equally")[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42763389/#short-view-affiliation-1 "Department of Radiation Oncology, Cancer Center & Institution of Stress Medicine, West China Hospital, Sichuan University, Chengdu, China."), [Jiayi Liu](https://pubmed.ncbi.nlm.nih.gov/?term=Liu+J&cauthor_id=42763389)[#](https://pubmed.ncbi.nlm.nih.gov/42763389/#short-view-equal-contrib-explanation "Contributed equally")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42763389/#short-view-affiliation-2 "Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China."), [Alifujiang Hairulajiang](https://pubmed.ncbi.nlm.nih.gov/?term=Hairulajiang+A&cauthor_id=42763389)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42763389/#short-view-affiliation-2 "Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China."), [Junjie Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+J&cauthor_id=42763389)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42763389/#short-view-affiliation-2 "Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China."), [Qianqian Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+Q&cauthor_id=42763389)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42763389/#short-view-affiliation-3 "Department of Oncology, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, Zhuzhou, China."), [ZhiHong Li](https://pubmed.ncbi.nlm.nih.gov/?term=Li+Z&cauthor_id=42763389)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42763389/#short-view-affiliation-4 "Department of Orthopaedics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China. lizhihong@csu.edu.cn.")[ 5 ](https://pubmed.ncbi.nlm.nih.gov/42763389/#short-view-affiliation-5 "Hunan Key Laboratory of Tumor Models and Individualized Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China. lizhihong@csu.edu.cn."), [Bingwen Zou](https://pubmed.ncbi.nlm.nih.gov/?term=Zou+B&cauthor_id=42763389)[ 6 ](https://pubmed.ncbi.nlm.nih.gov/42763389/#short-view-affiliation-6 "Department of Radiation Oncology, Cancer Center & Institution of Stress Medicine, West China Hospital, Sichuan University, Chengdu, China. zoubingwen81@163.com."), [Yeqian Feng](https://pubmed.ncbi.nlm.nih.gov/?term=Feng+Y&cauthor_id=42763389)[ 7 ](https://pubmed.ncbi.nlm.nih.gov/42763389/#short-view-affiliation-7 "Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China. fengyeqian@csu.edu.cn.") ### Affiliations * 1 Department of Radiation Oncology, Cancer Center & Institution of Stress Medicine, West China Hospital, Sichuan University, Chengdu, China. * 2 Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China. * 3 Department of Oncology, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, Zhuzhou, China. * 4 Department of Orthopaedics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China. lizhihong@csu.edu.cn. * 5 Hunan Key Laboratory of Tumor Models and Individualized Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China. lizhihong@csu.edu.cn. * 6 Department of Radiation Oncology, Cancer Center & Institution of Stress Medicine, West China Hospital, Sichuan University, Chengdu, China. zoubingwen81@163.com. * 7 Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China. fengyeqian@csu.edu.cn. # Contributed equally. * PMID: **42763389** * DOI: [ 10.1186/s12943-026-02786-4 ](https://doi.org/10.1186/s12943-026-02786-4) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID ## Abstract PD-1/PD-L1 blockade can produce durable tumor control, yet primary, adaptive, and acquired resistance remain common. Existing accounts often catalogue resistance by cellular compartment, obscuring the coordinated nature of tumor adaptation. Here, we introduce immune-pressure redistribution as a treatment-oriented framework that complements cancer immunoediting by asking where therapeutic immune pressure is diverted after checkpoint release. Resistance is organized into three coupled routes: transfer into tumor-intrinsic escape through antigen-presentation loss, interferon-response defects, oncogenic rewiring, and lineage plasticity; weakening through defective priming, terminal T-cell differentiation, compensatory checkpoints, metabolic constraint, and chronic cytokine signaling; and unloading into stromal, vascular, myeloid, regulatory, microbial, and systemic host compartments. We integrate clinically validated mechanisms with emerging evidence, including the temporal duality of interferon-JAK signaling, the role of tumor-draining lymph nodes in sustaining progenitor-exhausted T cells, and the limited translation of TIGIT, IDO1, TGF-β, and CSF-1R targeting. We further propose a biomarker-guided strategy that combines tumor visibility, immune-cell state, spatial architecture, systemic inflammation, and early treatment dynamics to identify the dominant resistance topology. This framework supports topology-matched combinations and adaptive sequencing rather than uniform escalation, with the aim of restoring productive immune pressure while limiting compensatory escape and toxicity. **Keywords:** Combination therapy; Immune-pressure redistribution; Immunotherapy resistance; PD-1/PD-L1 blockade; Predictive biomarkers. © 2026. The Author(s). [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declarations. Ethics approval and consent to participate: Not applicable. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests. ## References 1. 1. Rittmeyer A, et al. Atezolizumab versus docetaxel in patients with previously treated non-small-cell lung cancer (OAK): a phase 3, open-label, multicentre randomised controlled trial. Lancet. 2017;389(10066):255–65. - [PubMed](https://pubmed.ncbi.nlm.nih.gov/27979383/) - [DOI](https://doi.org/10.1016/s0140-6736\(16\)32517-x) 2. 1. Motzer RJ, et al. Nivolumab versus Everolimus in Advanced Renal-Cell Carcinoma. N Engl J Med. 2015;373(19):1803–13. - [PubMed](https://pubmed.ncbi.nlm.nih.gov/26406148/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/5719487/) - [DOI](https://doi.org/10.1056/nejmoa1510665) 3. 1. Robert C, et al. Pembrolizumab versus Ipilimumab in Advanced Melanoma. N Engl J Med. 2015;372(26):2521–32. - [PubMed](https://pubmed.ncbi.nlm.nih.gov/25891173/) - [DOI](https://doi.org/10.1056/nejmoa1503093) 4. 1. Regan MM, et al. Treatment-free survival over extended follow-up of patients with advanced melanoma treated with immune checkpoint inhibitors in CheckMate 067. J Immunother Cancer. 2021;9(11):e003743. - [PubMed](https://pubmed.ncbi.nlm.nih.gov/34799400/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/8606772/) - [DOI](https://doi.org/10.1136/jitc-2021-003743) 5. 1. Gettinger S, et al. Five-Year Follow-Up of Nivolumab in Previously Treated Advanced Non–Small-Cell Lung Cancer: Results From the CA209-003 Study. J Clin Oncol. 2018;36(17):1675–84. - [PubMed](https://pubmed.ncbi.nlm.nih.gov/29570421/) - [DOI](https://doi.org/10.1200/jco.2017.77.0412) Show all 251 references ## Publication types * Review Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Review%22%5Bpt%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Review) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42763389/) ## MeSH terms * Animals Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Animals%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Animals) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42763389/) * B7-H1 Antigen* / antagonists & inhibitors Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22B7-H1+Antigen%2Fantagonists+and+inhibitors%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=B7-H1+Antigen) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42763389/) * Biomarkers, Tumor* Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Biomarkers%2C+Tumor%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Biomarkers%2C+Tumor) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42763389/) * Drug Resistance, Neoplasm* / immunology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Drug+Resistance%2C+Neoplasm%2Fimmunology%22%5BMAJR%5D&
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