Evidence map›Paper›PMID 37809446›Full record

ArticleHeliyon2023

Engineering chimeric autoantibody receptor T cells for targeted B cell depletion in multiple sclerosis model: An

Maryam Sahlolbei, Mohammadreza Azangou-Khyavy, Javad Khanali, Babak Khorsand, Aref Shiralipour, Naser Ahmadbeigi, Zahra Madjd, Hossein Ghanbarian, Alireza Ardjmand, Seyed Mahmoud Hashemi and 1 more

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. CRISPR-Based Gene Therapy for Brain Disease.Molecular neurobiology · 2026
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  12. Article
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  15. Shifting gears with CAR T cells for autoimmune diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
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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

11 authors at 4 institutions in 2 countries.

Maryam SahlolbeiDepartment of Molecular Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences (IUMS), Tehran, Iran.
Mohammadreza Azangou-KhyavySchool of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Javad KhanaliSchool of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Babak KhorsandFoodborne and Waterborne Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Aref ShiralipourDepartment of Medical Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Naser AhmadbeigiGene Therapy Research Center, Digestive Disease Research Institute, Tehran University of Medical Sciences, Tehran, Iran.
Zahra MadjdOncopathology Research Center, Iran University of Medical Sciences, Tehran, Iran.
Hossein GhanbarianDepartment of Medical Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Alireza ArdjmandNSW Health Pathology, Sydney, New South Wales, Australia.
Seyed Mahmoud HashemiDepartment of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Jafar KianiDepartment of Molecular Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences (IUMS), Tehran, Iran.
Shahid Beheshti University of Medical Sciences · IRIran University of Medical Sciences · IRNew South Wales Department of Health · AUTehran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Recent evidence suggests that B cells and autoantibodies have a substantial role in the pathogenesis of Multiple sclerosis. T cells could be engineered to express chimeric autoantibody receptors (CAARs), which have an epitope of autoantigens in their extracellular domain acting as bait for trapping autoreactive B cells. This study aims to assess the function of designed CAAR T cells against B cell clones reactive to the myelin basic protein (MBP) autoantigen. Methods: T cells were transduced to express a CAAR consisting of MBP as the extracellular domain. experimental autoimmune encephalomyelitis (EAE) was induced by injecting MBP into mice. The cytotoxicity, proliferation, and cytokine production of the MBP-CAAR T cells were investigated in co-culture with B cells. Results: MBP-CAAR T cells showed higher cytotoxic activity against autoreactive B cells in all effector-to-target ratios compared to Mock T cell (empty vector-transduced T cell) and Un-T cells (un-transduced T cell). In co-cultures containing CAAR T cells, there was more proliferation and inflammatory cytokine release as compared to Un-T and Mock T cell groups. Conclusion: Based on these findings, CAAR T cells are promising for curing or modulating autoimmunity and can be served as a new approach for clone-specific B cell depletion therapy in multiple sclerosis.

Indexed as

Autoreactive B cellsChimeric autoantibody receptor (CAAR)Experimental autoimmune encephalomyelitis (EAE)Multiple sclerosis (MS)Myelin basic protein (MBP)

Identifiers

PMID37809446
PMCPMC10559048
OpenAlexW4386365501

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.