Evidence map›Paper›PMID 25943357›Full record

ArticleJournal of translational medicine2015

Development of genetically engineered iNKT cells expressing TCRs specific for the M. tuberculosis 38-kDa antigen.

Zhen-Min Jiang, Wei Luo, Qian Wen, Su-Dong Liu, Pei-Pei Hao, Chao-Ying Zhou, Ming-Qian Zhou, Li Ma

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Zhen-Min JiangInstitute of Molecular Immunology, School of Biotechnology, Southern Medical University, Guangzhou, 510515, China. jzhm0903@163.com.
Wei LuoInstitute of Molecular Immunology, School of Biotechnology, Southern Medical University, Guangzhou, 510515, China. luowei_421@163.com.
Qian WenInstitute of Molecular Immunology, School of Biotechnology, Southern Medical University, Guangzhou, 510515, China. wencaoxi@163.com.
Su-Dong LiuInstitute of Molecular Immunology, School of Biotechnology, Southern Medical University, Guangzhou, 510515, China. sudongliu@foxmail.com.
Pei-Pei HaoInstitute of Molecular Immunology, School of Biotechnology, Southern Medical University, Guangzhou, 510515, China. haopei_2008@126.com.
Chao-Ying ZhouInstitute of Molecular Immunology, School of Biotechnology, Southern Medical University, Guangzhou, 510515, China. zhouchaoying100@163.com.
Ming-Qian ZhouInstitute of Molecular Immunology, School of Biotechnology, Southern Medical University, Guangzhou, 510515, China. zmq12@163.com.
Li MaInstitute of Molecular Immunology, School of Biotechnology, Southern Medical University, Guangzhou, 510515, China. maryhmz@126.com.
Southern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe invariant natural killer T (iNKT) cell has been shown to play a central role in early stages immune responses against Mycobacterium tuberculosis (Mtb) infection, which become nonresponsive (anergic) and fails to control the growth of Mtb in patients with active tuberculosis. Enhancement of iNKT cell responses to Mtb antigens can help to resist infection. STUDY DESIGN AND

methodsIn the present study, an Mtb 38-kDa antigen-specific T cell receptor (TCR) was isolated from human CD8(+) T cells stimulated by 38-kDa antigen in vitro, and then transduced into primary iNKT cells by retrovirus vector.

resultsThe TCR gene-modified iNKT cells are endowed with new features to behave as a conventional MHC class I restricted CD8(+) T lymphocyte by displaying specific antigen recognition and anti-Mtb antigen activity in vitro. At the same time, the engineered iNKT cells retaining its original capacity to be stimulated proliferation by non-protein antigens α-Gal-Cer.

conclusionsThis work is the first attempt to engineer iNKT cells by exogenous TCR genes and demonstrated that iNKT cell, as well as CD4(+) and CD8(+) T cells, can be genetically engineered to confer them a defined and alternative specificity, which provides new insights into TCR gene therapy for tuberculosis patients, especially those infected with drug-resistant Mtb.

Indexed as

Antibodies, MonoclonalAntigens, BacterialCD8-Positive T-LymphocytesCell ProliferationCytokinesGenetic EngineeringHealthy VolunteersHLA-A AntigensHumansLipoproteinsLymphocyte ActivationMicroscopy, FluorescenceMycobacterium tuberculosisNatural Killer T-CellsNormal DistributionReceptors, Antigen, T-CellAg38 antigen, Mycobacterium tuberculosisAntibodies, MonoclonalAntigens, BacterialCytokinesHLA-A AntigensLipoproteinsReceptors, Antigen, T-Cell

Identifiers

PMID25943357
PMCPMC4428004
OpenAlexW1526769731

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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.