Evidence map›Paper›PMID 34323289›Full record

ArticleEuropean journal of immunology2021

Mutant B2M-HLA-E and B2M-HLA-G fusion proteins protects universal chimeric antigen receptor-modified T cells from allogeneic NK cell-mediated lysis.

Yelei Guo, Beilei Xu, Zhiqiang Wu, Jian Bo, Chuan Tong, Deyun Chen, Jin Wang, Haoyi Wang, Yao Wang, Weidong Han

Open access · hybridAbstract read
In one paragraph

Article in European journal of immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.0field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
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

10 authors at 2 institutions in 1 country.

Yelei GuoDepartment of Bio-therapeutic, the First Medical Centre, Chinese PLA General Hospital, Beijing, China.
Beilei XuState Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Zhiqiang WuDepartment of Bio-therapeutic, the First Medical Centre, Chinese PLA General Hospital, Beijing, China.
Jian BoDepartment of Hematology, the First Medical Centre, Chinese PLA General Hospital, Beijing, China.
Chuan TongDepartment of Bio-therapeutic, the First Medical Centre, Chinese PLA General Hospital, Beijing, China.
Deyun ChenDepartment of Bio-therapeutic, the First Medical Centre, Chinese PLA General Hospital, Beijing, China.
Jin WangDepartment of Outpatient, the Sixth Medical Centre, Chinese PLA General Hospital, Beijing, China.
Haoyi WangState Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Yao WangDepartment of Bio-therapeutic, the First Medical Centre, Chinese PLA General Hospital, Beijing, China.
Weidong HanDepartment of Bio-therapeutic, the First Medical Centre, Chinese PLA General Hospital, Beijing, China.
Chinese PLA General Hospital · CNInstitute of Zoology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have indicated the antitumor activity and reduced allogeneic response of universal chimeric antigen receptor-modified T (UCAR T) cells lacking endogenous T cell receptors and beta-2 microglobulin (B2M) generated using gene-editing technologies. However, these cells are vulnerable to lysis by allogeneic natural killer (NK) cells due to their lack of human leukocyte antigen (HLA) class I molecule expression. Here, constitutive expression of mutant B2M-HLA-E (mBE) and B2M-HLA-G (mBG) fusion proteins in anti-CD19 UCAR T (UCAR T-19) cells was conducted to protect against allogeneic NK cell-mediated lysis. The ability of cells expressing mBE or mBG to resist NK cell-mediated lysis was observed in gene-edited Jurkat CAR19 cells. UCAR T-19 cells constitutively expressing the mBE and mBG fusion proteins were manufactured and showed effective and specific anti-tumor activity. Constitutive expression of the mBE and mBG fusion proteins in UCAR T-19 cells prevented allogeneic NK cell-mediated lysis. In addition, these cells were not recognizable by allogeneic T cells. Additional experiments, including those in animal models and clinical trials, are required to evaluate the safety and efficacy of UCAR T-19 cells that constitutively express mBE and mBG.

Indexed as

MutationAntigens, CD19beta 2-MicroglobulinCytotoxicity, ImmunologicGene Knockout TechniquesHistocompatibility Antigens Class IHLA-E AntigensHLA-G AntigensHumansImmunophenotypingKiller Cells, NaturalLymphocyte ActivationReceptors, Antigen, T-CellReceptors, Chimeric AntigenT-LymphocytesAntigens, CD19B2M protein, humanbeta 2-MicroglobulinHistocompatibility Antigens Class IHLA-E AntigensHLA-G AntigensReceptors, Antigen, T-CellReceptors, Chimeric Antigenchimeric antigen receptorHLA-EHLA-GNK cellsuniversal CAR T

Identifiers

PMID34323289
PMCPMC9292285
OpenAlexW3184752971

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.