Evidence map›Paper›PMID 38299614›Full record

ArticleHaematologica2024

GPIbα CAAR T cells function like a Trojan horse to eliminate autoreactive B cells to treat immune thrombocytopenia.

Jie Zhou, Yanyan Xu, Jinhui Shu, Haojie Jiang, Linlin Huang, Min Xu, Junling Liu, Yu Hu, Heng Mei

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 6 citations in OpenAlex.

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  14. Synergistic integration of mRNA-LNP with CAR-engineered immune cells: Pioneering progress in immunotherapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
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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

9 authors at 5 institutions in 1 country.

Jie ZhouInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan 430022, Hubei, China; Hubei Clinical Medical Center of Cell Therapy for Neoplastic Disease, Wuhan,430022.
Yanyan XuDepartment of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Rd, Shanghai 200025.
Jinhui ShuInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan 430022, Hubei, China; Hubei Clinical Medical Center of Cell Therapy for Neoplastic Disease, Wuhan,430022.
Haojie JiangDepartment of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Rd, Shanghai 200025.
Linlin HuangInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan 430022, Hubei, China; Hubei Clinical Medical Center of Cell Therapy for Neoplastic Disease, Wuhan,430022.
Min XuInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan 430022, Hubei, China; Hubei Clinical Medical Center of Cell Therapy for Neoplastic Disease, Wuhan,430022.
Junling LiuDepartment of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Rd, Shanghai 200025.
Yu HuInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan 430022, Hubei, China; Hubei Clinical Medical Center of Cell Therapy for Neoplastic Disease, Wuhan,430022. dr_huyu@126.com.
Heng MeiInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan 430022, Hubei, China; Hubei Clinical Medical Center of Cell Therapy for Neoplastic Disease, Wuhan,430022. hmei@hust.edu.cn.
Shanghai Jiao Tong University · CNHubei Cancer Hospital · CNUnion Hospital · CNHuazhong University of Science and Technology · CNWuhan Union Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breakthrough treatment for refractory and relapsed immune thrombocytopenia (ITP) patients is urgently needed. Autoantibody- mediated platelet clearance and megakaryocyte dysfunction are important pathogenic mediators of ITP. Glycoprotein (GP) Ibα is a significant autoantigen found in ITP patients and is associated with poor response to standard immunosuppressive treatments. Here, we engineered human T cells to express a chimeric autoantibody receptor (CAAR) with GPIbα constructed into the ligand-binding domain fused to the CD8 transmembrane domain and CD3ζ-4-1BB signaling domains. We performed cytotoxicity assays to assess GPIbα CAAR T-cell selective cytolysis of cells expressing anti-GPIbα B-cell receptors in vitro. Furthermore, we demonstrated the potential of GPIbα CAAR T cells to persist and precisely eliminate GPIbα-specific B cells in vivo. In summary, we present a proof of concept for CAAR T-cell therapy to eradicate autoimmune B cells while sparing healthy B cells with GPIbα CAAR T cells that function like a Trojan horse. GPIbα CAAR T-cell therapy is a promising treatment for refractory and relapsed ITP patients.

Indexed as

B-LymphocytesPlatelet Glycoprotein GPIb-IX ComplexPurpura, Thrombocytopenic, IdiopathicT-LymphocytesAnimalsAutoantibodiesAutoimmunityHumansMiceReceptors, Chimeric Antigenadhesion receptorAutoantibodiesPlatelet Glycoprotein GPIb-IX ComplexReceptors, Chimeric Antigen

Identifiers

PMID38299614
PMCPMC11215394
OpenAlexW4391448381

What OpenQuestion holds

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LicenceCC BY-NC
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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 OpenQuestion graph.