Evidence map›Paper›PMID 37161050›Full record

ArticleCommunications biology2023

Anti-human-TIGIT agonistic antibody ameliorates autoimmune diseases by inhibiting Tfh and Tph cells and enhancing Treg cells.

Marenori Kojima, Katsuya Suzuki, Masaru Takeshita, Masaki Ohyagi, Mana Iizuka, Humitsugu Yamane, Keiko Koga, Taku Kouro, Yoshiaki Kassai, Tomoki Yoshihara and 8 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. PD1RMD open · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Reduced TIGITClinical rheumatology · 2025
    Article
  9. Article
  10. Review
  11. Review
  12. Occurrence and role of Tph cells in various renal diseases.Molecular medicine (Cambridge, Mass.) · 2024
    Review
  13. Review
  14. Review
  15. 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

18 authors at 3 institutions in 1 country.

Marenori KojimaDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.ORCID 0000-0001-7637-4867
Katsuya SuzukiDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Masaru TakeshitaDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Masaki OhyagiDepartment of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Mana IizukaDepartment of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Humitsugu YamaneDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Keiko KogaImmunology Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa City, Kanagawa, Japan.
Taku KouroImmunology Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa City, Kanagawa, Japan.
Yoshiaki KassaiImmunology Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa City, Kanagawa, Japan.
Tomoki YoshiharaBiomolecular Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa City, Kanagawa, Japan.
Ryutaro AdachiBiomolecular Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa City, Kanagawa, Japan.
Kentarou HashikamiBiomolecular Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa City, Kanagawa, Japan.
Yuichiro OtaDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Keiko YoshimotoDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Yuko KanekoDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Rimpei MoritaDepartment of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Akihiko YoshimuraDepartment of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Tsutomu TakeuchiDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan. tsutake@z5.keio.jp.ORCID 0000-0003-1111-8218
Keio University · JPTakeda (Japan) · JPFujisawa City Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T cells play important roles in autoimmune diseases, but it remains unclear how to optimally manipulate them. We focused on the T cell immunoreceptor with Ig and ITIM domains (TIGIT), a coinhibitory molecule that regulates and is expressed in T cells. In autoimmune diseases, the association between TIGIT-expressing cells and pathogenesis and the function of human-TIGIT (hu-TIGIT) signalling modification have not been fully elucidated. Here we generated anti-hu-TIGIT agonistic monoclonal antibodies (mAbs) and generated hu-TIGIT knock-in mice to accurately evaluate the efficacy of mAb function. Our mAb suppressed the activation of CD4

Indexed as

Autoimmune DiseasesT-Lymphocytes, RegulatoryAnimalsAntibodies, MonoclonalMiceReceptors, ImmunologicSignal TransductionAntibodies, MonoclonalReceptors, Immunologic

Identifiers

PMID37161050
PMCPMC10170076
OpenAlexW4376114595

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.