Evidence map›Paper›PMID 42664956›Full record

ArticleCell reports. Medicine2026

Inhibition of the lipocalin-2-phosphatidylserine axis restores natural killer cell immune surveillance.

Jingkun Qin, Xinyu Hu, Lei Wang, Ying Cai, Ziming Hu, Xiuxiu Xu, Zhigang Nian, Zhenbang Liu, Xiaoyu Ding, Yan Jiang and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports. Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Jingkun QinNational Key Laboratory of Immune Response and Immunotherapy, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Institute of Immunology, Biomedical Sciences and Health Laboratory of Anhui Province, University of Science and Technology of China, Hefei, China.
Xinyu HuNational Key Laboratory of Immune Response and Immunotherapy, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Institute of Immunology, Biomedical Sciences and Health Laboratory of Anhui Province, University of Science and Technology of China, Hefei, China.
Lei WangThe First Affiliated Hospital of University of Science and Technology of China, Division of Life Science and Medicine, University of Science and Technology of China, Hefei, China; Ministry of Education Key Laboratory for Membrane-less Organelles & Cellular Dynamics, Hefei National Laboratory for Physical Sciences at the Microscale, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Ying CaiThe First Affiliated Hospital of University of Science and Technology of China, Division of Life Science and Medicine, University of Science and Technology of China, Hefei, China.
Ziming HuNational Key Laboratory of Immune Response and Immunotherapy, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Institute of Immunology, Biomedical Sciences and Health Laboratory of Anhui Province, University of Science and Technology of China, Hefei, China.
Xiuxiu XuInstitute of Immunology, Biomedical Sciences and Health Laboratory of Anhui Province, University of Science and Technology of China, Hefei, China.
Zhigang NianNational Key Laboratory of Immune Response and Immunotherapy, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Institute of Immunology, Biomedical Sciences and Health Laboratory of Anhui Province, University of Science and Technology of China, Hefei, China.
Zhenbang LiuNational Key Laboratory of Immune Response and Immunotherapy, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Xiaoyu DingNational Key Laboratory of Immune Response and Immunotherapy, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Institute of Immunology, Biomedical Sciences and Health Laboratory of Anhui Province, University of Science and Technology of China, Hefei, China.
Yan JiangNational Key Laboratory of Immune Response and Immunotherapy, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Institute of Immunology, Biomedical Sciences and Health Laboratory of Anhui Province, University of Science and Technology of China, Hefei, China.
Yuanhao LinNational Key Laboratory of Immune Response and Immunotherapy, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Institute of Immunology, Biomedical Sciences and Health Laboratory of Anhui Province, University of Science and Technology of China, Hefei, China.
Ke RuanThe First Affiliated Hospital of University of Science and Technology of China, Division of Life Science and Medicine, University of Science and Technology of China, Hefei, China; Ministry of Education Key Laboratory for Membrane-less Organelles & Cellular Dynamics, Hefei National Laboratory for Physical Sciences at the Microscale, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Binqing FuNational Key Laboratory of Immune Response and Immunotherapy, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Institute of Immunology, Biomedical Sciences and Health Laboratory of Anhui Province, University of Science and Technology of China, Hefei, China; The First Affiliated Hospital of University of Science and Technology of China, Division of Life Science and Medicine, University of Science and Technology of China, Hefei, China.
Zhigang TianNational Key Laboratory of Immune Response and Immunotherapy, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Institute of Immunology, Biomedical Sciences and Health Laboratory of Anhui Province, University of Science and Technology of China, Hefei, China.
Yonggang ZhouNational Key Laboratory of Immune Response and Immunotherapy, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Institute of Immunology, Biomedical Sciences and Health Laboratory of Anhui Province, University of Science and Technology of China, Hefei, China; The First Affiliated Hospital of University of Science and Technology of China, Division of Life Science and Medicine, University of Science and Technology of China, Hefei, China. Electronic address: ygzhou@ustc.edu.cn.
Haiming WeiNational Key Laboratory of Immune Response and Immunotherapy, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Institute of Immunology, Biomedical Sciences and Health Laboratory of Anhui Province, University of Science and Technology of China, Hefei, China; The First Affiliated Hospital of University of Science and Technology of China, Division of Life Science and Medicine, University of Science and Technology of China, Hefei, China; Center for Advanced Interdisciplinary Science and Biomedicine of IHM, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230027, China. Electronic address: ustcwhm@ustc.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipid metabolic reprogramming can facilitate immune escape by promoting a suppressive phenotype in tumor-infiltrating immune cells, although this process remains poorly understood. Here, we identify the lipoprotein, Lipocalin-2 (LCN2), as an essential factor driving natural killer (NK) cell dysfunction and immunosuppressive phenotype. Spatial metabolomics with crystal structure analysis demonstrates that LCN2 binding to phosphatidylserine (PS) and PS enrichment is required for tumor-associated lipid reprogramming. Increased LCN2-PS binding limits IL-15-mediated JAK-STAT pathway activation in NK cells, while inhibiting tumor-infiltrating neutrophil maintenance of anti-tumor potential in NK cells via suppression of IFN-I response. Structure-based drug screening identifies semapimod as an LCN2 inhibitor that blocks interaction with PS, disrupting the LCN2-PS immunosuppressive axis and inducing tumor control. Overall, this study uncovers a lipid metabolic reprogramming mechanism that mediates innate immune evasion and proposes a tumor treatment strategy through enhanced innate immune surveillance.

Indexed as

Immunologic SurveillanceKiller Cells, NaturalLipocalin-2PhosphatidylserinesAnimalsHumansMetabolic ReprogrammingMiceSignal TransductionLipocalin-2Phosphatidylserinesimmune evasionimmunotherapylipid metabolismlipocalin-2NK cell exhaustionphosphatidylserinetumor microenvironment

Identifiers

PMID42664956
PMCPMC13589504

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.