Evidence map›Paper›PMID 38780694›Full record

ReviewInflammation2025

TIGIT Regulates T Cell Inflammation in Airway Inflammatory Diseases.

Junyi Ke, Shu Huang, Zhixiong He, Siyu Lei, Shiya Lin, Minchao Duan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation, 2025. 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
–field-weighted citation impact
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.

  1. Observational
  2. Immune checkpoint molecules beyond PD-1 and CTLA-4: emerging targets in autoimmune diseases and cancer immunotherapy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. 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

6 authors.

Junyi KeGuangxi Medical University, Nanning, China.
Shu HuangWuming Hospital of Guangxi Medical University, Nanning, China.
Zhixiong HeGuangxi Medical University, Nanning, China.
Siyu LeiWuming Hospital of Guangxi Medical University, Nanning, China.
Shiya LinGuangxi Medical University, Nanning, China.
Minchao DuanWuming Hospital of Guangxi Medical University, Nanning, China. 731321667@qq.com.

Funding

National Natural Science Foundation of China 82260011
6 · The paper itself

Abstract

TIGIT, a co-inhibitory receptor found on T cells and NK cells, transmits inhibitory signals upon binding to its ligand. This interaction suppresses the activation of various signaling pathways, leading to functional exhaustion of cells, ultimately dampening excessive inflammatory responses or facilitating immune evasion in tumors. Dysregulated TIGIT expression has been noted in T cells across different inflammatory conditions, exhibiting varying effects based on T cell subsets. TIGIT predominantly restrains the effector function of pro-inflammatory T cells, upholds the suppressive function of regulatory T cells, and influences Tfh maturation. Mechanistically, the IL27-induced transcription factors c-Maf and Blimp-1 are believed to be key regulators of TIGIT expression in T cells. Notably, TIGIT expression in T cells is implicated in lung diseases, particularly airway inflammatory conditions such as lung cancer, obstructive pulmonary disease, interstitial lung disease, sarcoidosis, and COVID-19. This review emphasizes the significance of TIGIT in the context of T cell immunity and airway inflammatory diseases.

Indexed as

InflammationLung DiseasesReceptors, ImmunologicT-LymphocytesAnimalsCOVID-19HumansReceptors, ImmunologicTIGIT protein, humanairway inflammatory diseaseimmunityinflammationT cellsTIGIT

Identifiers

What Socratic holds

Textmetadata
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 Socratic graph.