Evidence map›Paper›PMID 32771992›Full record

ArticleJournal for immunotherapy of cancer2020

Antagonistic anti-LILRB1 monoclonal antibody regulates antitumor functions of natural killer cells.

Heyu Chen, Yuanzhi Chen, Mi Deng, Samuel John, Xun Gui, Ankit Kansagra, Weina Chen, Jaehyup Kim, Cheryl Lewis, Guojin Wu and 12 more

Open access · goldAbstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.7field-weighted citation impact, top 9% of its field
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

41 citing papers in PubMed, 59 citations in OpenAlex.

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  11. A Switch Protein Adapter for Anti-LILRB4 CAR-T Cells.European journal of immunology · 2025
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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

22 authors at 6 institutions in 3 countries.

Heyu Chen *Department of Physiology, UT Southwestern Medical Center, Dallas, Texas, USA.ORCID 0000-0001-8842-8586
Yuanzhi Chen *Texas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Mi DengDepartment of Physiology, UT Southwestern Medical Center, Dallas, Texas, USA.
Samuel JohnDepartment of Pediatrics, Pediatric Hematology- Oncology, UT Southwestern Medical Center, Dallas, Texas, USA.
Xun GuiTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Ankit KansagraDepartment of Hematology and Oncology, UT Southwestern Medical Center, Dallas, Texas, USA.
Weina ChenDepartment of Pathology, UT Southwestern Medical Center, Dallas, Texas, USA.
Jaehyup KimDepartment of Pathology, UT Southwestern Medical Center, Dallas, Texas, USA.
Cheryl LewisHarold C. Simmons Comprehensive Cancer Center, UT Southwestern Medical Center, Dallas, Texas, USA.
Guojin WuDepartment of Physiology, UT Southwestern Medical Center, Dallas, Texas, USA.
Jingjing XieDepartment of Physiology, UT Southwestern Medical Center, Dallas, Texas, USA.
Lingbo ZhangDepartment of Physiology, UT Southwestern Medical Center, Dallas, Texas, USA.
Ryan HuangDepartment of Physiology, UT Southwestern Medical Center, Dallas, Texas, USA.
Xiaoye LiuDepartment of Physiology, UT Southwestern Medical Center, Dallas, Texas, USA.
Hisashi AraseDepartment of Immunochemistry, Research Institute for Microbial Diseases and Laboratory of Immunochemistry, World Premier International Immunology Frontier Research Center, Osaka University, Osaka, Japan.
Yang HuangSchool of Public Health, Xiamen University, Xiamen, Fujian, China.
Hai YuSchool of Public Health, Xiamen University, Xiamen, Fujian, China.
Wenxin LuoSchool of Public Health, Xiamen University, Xiamen, Fujian, China.
Ningshao XiaSchool of Public Health, Xiamen University, Xiamen, Fujian, China.ORCID 0000-0003-0179-5266
Ningyan ZhangTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA Alec.Zhang@UTSouthwestern.edu Ningyan.Zhang@uth.tmc.edu Zhiqiang.An@uth.tmc.edu.
Zhiqiang AnTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA Alec.Zhang@UTSouthwestern.edu Ningyan.Zhang@uth.tmc.edu Zhiqiang.An@uth.tmc.edu.
Cheng Cheng ZhangDepartment of Physiology, UT Southwestern Medical Center, Dallas, Texas, USA Alec.Zhang@UTSouthwestern.edu Ningyan.Zhang@uth.tmc.edu Zhiqiang.An@uth.tmc.edu.
Southwestern Medical Center · USXiamen University · CNBrown Foundation · USCentral South University · CNOsaka International University · JPSouthwestern Medical Center

Funding

UT Southwestern Medical Center Simmons Comprehensive Cancer CenterP30CA142543 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI Sandi Leigh Pruitt · 2010 to 2026
$53.7M
INTEGRATIVE IMMUNOLOGY TRAINING PROGRAMT32AI005284 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Nan Yan · 2003 to 2026
$7.4M
ITIM-receptors for cancer treatmentR01CA248736 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI ZHANG, CHENGCHENG · 2020 to 2024
$2.9M
NCI NIH HHS P30 CA142543NCI NIH HHS R01 CA248736NIAID NIH HHS T32 AI005284
6 · The paper itself

Abstract

backgroundCurrent immune checkpoint blockade strategies have been successful in treating certain types of solid cancer. However, checkpoint blockade monotherapies have not been successful against most hematological malignancies including multiple myeloma and leukemia. There is an urgent need to identify new targets for development of cancer immunotherapy. LILRB1, an immunoreceptor tyrosine-based inhibitory motif-containing receptor, is widely expressed on human immune cells, including B cells, monocytes and macrophages, dendritic cells and subsets of natural killer (NK) cells and T cells. The ligands of LILRB1, such as major histocompatibility complex (MHC) class I molecules, activate LILRB1 and transduce a suppressive signal, which inhibits the immune responses. However, it is not clear whether LILRB1 blockade can be effectively used for cancer treatment.

methodsFirst, we measured the LILRB1 expression on NK cells from cancer patients to determine whether LILRB1 upregulated on NK cells from patients with cancer, compared with NK cells from healthy donors. Then, we developed specific antagonistic anti-LILRB1 monoclonal antibodies and studied the effects of LILRB1 blockade on the antitumor immune function of NK cells, especially in multiple myeloma models,

resultsWe demonstrate that percentage of LILRB1

conclusionsOur results indicate that blocking LILRB1 signaling on immune effector cells such as NK cells may represent a novel strategy for the development of anticancer immunotherapy.

Indexed as

AnimalsAntibodies, MonoclonalFemaleHumansKiller Cells, NaturalLeukocyte Immunoglobulin-like Receptor B1MiceMice, Inbred NODAntibodies, MonoclonalLeukocyte Immunoglobulin-like Receptor B1antibodies, neoplasmcytotoxicity, immunologicimmunotherapykiller cells, naturalreceptors, immunologic

Identifiers

PMID32771992
PMCPMC7418854
OpenAlexW3047797642

What OpenQuestion holds

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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.