Evidence map›Paper›PMID 35090381›Full record

ArticlemAbs

Structural and functional characterization of a monoclonal antibody blocking TIGIT.

Bo-Seong Jeong, Hyemi Nam, Jeewon Lee, Hye-Young Park, Ki Joon Cho, Joong Hyuk Sheen, Eunjung Song, Meesook Oh, Sunggeun Lee, Hyemin Choi and 3 more

Open access · goldAbstract read
In one paragraph

Article in mAbs. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Multiple myeloma and the potential of new checkpoint inhibitors for immunotherapy.Therapeutic advances in vaccines and immunotherapy · 2024
    Review
  10. Review
  11. Article
  12. Article
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

13 authors at 2 institutions in 2 countries.

Bo-Seong JeongDepartment of Biological Sciences, Kaist Institute for the Biocentury, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea.ORCID 0000-0003-0629-6722
Hyemi NamDepartment of Target ID & Assay Development, Mogam Institute for Biomedical Research, Gyeonggi-do, Republic of Korea.
Jeewon LeeDepartment of Target ID & Assay Development, Mogam Institute for Biomedical Research, Gyeonggi-do, Republic of Korea.
Hye-Young ParkDepartment of Target ID & Assay Development, Mogam Institute for Biomedical Research, Gyeonggi-do, Republic of Korea.
Ki Joon ChoDepartment of Target ID & Assay Development, Mogam Institute for Biomedical Research, Gyeonggi-do, Republic of Korea.
Joong Hyuk SheenDepartment of Target ID & Assay Development, Mogam Institute for Biomedical Research, Gyeonggi-do, Republic of Korea.
Eunjung SongDepartment of Protein Engineering, Mogam Institute for Biomedical Research, Gyeonggi-do, Republic of Korea.
Meesook OhDepartment of Research and Early Development, Gc Pharma, Gyeonggi-do, Republic of Korea.
Sunggeun LeeDepartment of Research and Early Development, Gc Pharma, Gyeonggi-do, Republic of Korea.
Hyemin ChoiDepartment of Research and Early Development, Gc Pharma, Gyeonggi-do, Republic of Korea.
Jung-Eun YangDepartment of Research and Early Development, Gc Pharma, Gyeonggi-do, Republic of Korea.
Munkyung KimDepartment of Target ID & Assay Development, Mogam Institute for Biomedical Research, Gyeonggi-do, Republic of Korea.
Byung-Ha OhDepartment of Biological Sciences, Kaist Institute for the Biocentury, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea.ORCID 0000-0002-6437-8470
Target (United States) · USKorea Advanced Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TIGIT is an immune checkpoint receptor that is expressed on subsets of activated T cells and natural killer (NK) cells. Several ligands for TIGIT, including poliovirus receptor (PVR), are expressed on cancer cells and mediate inhibitory signaling to suppress antitumor activities of the immune cells. Many studies support that the TIGIT signaling is a potential target for cancer immunotherapy. We developed an IgG4-type monoclonal antibody against human TIGIT, designated as MG1131, using a phage display library of single-chain variable fragments (scFvs). MG1131 interacts with TIGIT much more tightly than PVR does. The crystal structure of a scFv version of MG1131 bound to TIGIT was determined, showing that MG1131 could block the PVR-TIGIT interaction and thus the immunosuppressive signaling of TIGIT. Consistently, MG1131 is bound to TIGIT-expressing cells and interferes with PVR binding to these cells. Moreover, MG1131 increased NK cell-mediated tumor killing activities, inhibited immunosuppressive activity of regulatory T (Treg) cells from healthy donors, and restored interferon-γ secretion from peripheral blood mononuclear cells derived from multiple myeloma patients. MG1131 also increased T cell infiltration to the tumor site and inhibited tumor growth in mice. Collectively, these data indicate that MG1131 modulates the effector functions of T cells and NK cells positively and Treg cells negatively.

Indexed as

Cell Surface Display TechniquesAntibodies, NeutralizingHumansReceptors, ImmunologicSingle-Chain AntibodiesAntibodies, NeutralizingReceptors, ImmunologicSingle-Chain AntibodiesTIGIT protein, humanCancercrystal structureimmune checkpointmonoclonal antibodyTIGIT

Identifiers

PMID35090381
PMCPMC8803117
OpenAlexW4210318020

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.