Evidence map›Paper›PMID 39231544›Full record

ArticleJournal for immunotherapy of cancer2024

Targeting IL-33 reprograms the tumor microenvironment and potentiates antitumor response to anti-PD-L1 immunotherapy.

Yanyang Nan, Yu Bai, Xiaozhi Hu, Kaicheng Zhou, Tao Wu, An Zhu, Mengyang Li, Zihan Dou, Zhonglian Cao, Xumeng Zhang and 8 more

Erratum issuedAbstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
–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

16 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  4. Targeting IL-33 in Precision Neuroimmunology: Cellular Mechanisms and Therapeutic Strategies for CNS Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors.

Yanyang Nan *Department of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.
Yu Bai *Department of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.
Xiaozhi Hu *Department of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.
Kaicheng Zhou *Department of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.
Tao WuDepartment of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.
An ZhuDepartment of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.
Mengyang LiDepartment of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.
Zihan DouDepartment of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.
Zhonglian CaoDepartment of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.
Xumeng ZhangCollege of Literature, Science, and the Arts, University of Michigan, Ann Arbor, Michigan, USA.
Shuwen XuDepartment of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.
Yuanzhen ZhangDepartment of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.
Jun LinDepartment of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.
Xian ZengDepartment of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.
Jiajun FanDepartment of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.
Xuyao ZhangDepartment of pharmacy, Shanghai Children’s Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, China dianwenju@fudan.edu.cn binxuewang@sjtu.edu.cn xuyaozhang@fudan.edu.cn.ORCID 0000-0003-1654-5550
Xuebin WangShanghai Jiao Tong University, Shanghai, China dianwenju@fudan.edu.cn binxuewang@sjtu.edu.cn xuyaozhang@fudan.edu.cn.
Dianwen JuDepartment of pharmacy, Shanghai Children’s Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, China dianwenju@fudan.edu.cn binxuewang@sjtu.edu.cn xuyaozhang@fudan.edu.cn.ORCID 0000-0002-4305-9622

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe main challenge against patients with cancer to derive benefits from immune checkpoint inhibitors targeting PD-1/PD-L1 appears to be the immunosuppressive tumor microenvironment (TME), in which IL-33/ST2 signal fulfills critical functions. However, whether IL-33 limits the therapeutic efficacy of anti-PD-L1 remains uncertain.

methodsMolecular mechanisms of IL-33/ST2 signal on anti-PD-L1 treatment lewis lung carcinoma tumor model were assessed by RNA-seq, ELISA, WB and immunofluorescence (IF). A sST2-Fc fusion protein was constructed for targeting IL-33 and combined with anti-PD-L1 antibody for immunotherapy in colon and lung tumor models. On this basis, bifunctional fusion proteins were generated for PD-L1-targeted blocking of IL-33 in tumors. The underlying mechanisms of dual targeting of IL-33 and PD-L1 revealed by RNA-seq, scRNA-seq, FACS, IF and WB.

resultsAfter anti-PD-L1 administration, tumor-infiltrating ST2

conclusionsIn this study, we demonstrated that IL-33/ST2 was involved in the immunosuppression mechanism of PD-L1 antibody therapy, and blockade by sST2-Fc or anti-PD-L1-sST2 could remodel the inflammatory TME and induce potent antitumor effect, highlighting the potential therapeutic strategies for the tumor treatment by simultaneously targeting IL-33 and PD-L1.

Indexed as

ImmunotherapyInterleukin-33Tumor MicroenvironmentAnimalsB7-H1 AntigenCell Line, TumorHumansImmune Checkpoint InhibitorsInterleukin-1 Receptor-Like 1 ProteinMiceMice, Inbred C57BLB7-H1 AntigenCd274 protein, mouseImmune Checkpoint InhibitorsInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Immune Checkpoint InhibitorImmune modulatoryImmunotherapyT regulatory cell - TregTumor microenvironment - TME

Identifiers

PMID39231544
PMCPMC11409265

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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.