Evidence map›Paper›PMID 41805925›Full record

ArticleCancer immunology, immunotherapy : CII2026

Protein-level profiling of TIGIT axis components in human PDAC reveals immune-suppressive expression patterns.

D Quatannens, Y Verhoeven, S van der Heijden, D Peeters, J Claes, C Hermans, H Lambrechts, K Zwaenepoel, P van Dam, M Peeters and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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.

D QuatannensCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, Antwerp, Belgium.
Y VerhoevenCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, Antwerp, Belgium.
S van der HeijdenCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, Antwerp, Belgium.
D PeetersDepartment of Pathology, Antwerp University Hospital (UZA), Antwerp, Belgium.
J ClaesData Science Institute, I-Biostat, Hasselt University, Hasselt, Belgium.
C HermansCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, Antwerp, Belgium.
H LambrechtsCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, Antwerp, Belgium.
K ZwaenepoelDepartment of Pathology, Antwerp University Hospital (UZA), Antwerp, Belgium.
P van DamCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, Antwerp, Belgium.
M PeetersCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, Antwerp, Belgium.
H PrenenCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, Antwerp, Belgium.
S KoljenovicCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, Antwerp, Belgium.
J De WaeleCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, Antwerp, Belgium.
C FaesData Science Institute, I-Biostat, Hasselt University, Hasselt, Belgium.
F LardonCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, Antwerp, Belgium.
G RoeyenDepartment of Hepatobiliary Transplantation and Endocrine Surgery, Antwerp University Hospital (UZA), Antwerp, Belgium.
E SmitsCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, Antwerp, Belgium.
J Van AudenaerdeCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, Antwerp, Belgium. jonas.vanaudenaerde@uantwerpen.be.

Funding

Fonds Wetenschappelijk Onderzoek 1S69721NFonds Wetenschappelijk Onderzoek 1S76421N
6 · The paper itself

Abstract

purposeIn pancreatic ductal adenocarcinoma (PDAC), immune checkpoint inhibitors have shown limited efficacy, and the role of the TIGIT axis remains underexplored. This study aimed to characterize TIGIT axis components on protein level and their relationship to PD-1/PD-L1 expression in matched blood and tumor samples from PDAC patients to identify immunosuppressive mechanisms and fuel future strategies for immune checkpoint co-targeting in PDAC patients. EXPERIMENTAL

designFresh tumor and peripheral blood samples were collected from PDAC patients undergoing surgical resection. Flow cytometry was performed on tumor-infiltrating lymphocytes and PBMCs to assess expression of TIGIT, DNAM-1, TACTILE, and PD-1. Ligands CD111, CD112, CD113, and CD155 were analyzed using immunohistochemistry. Additional RNA expression analysis (TCGA/GTEx) was used to evaluate ligand distribution and gene expression profiles.

resultsTIGIT was highly upregulated on intratumoral CD8⁺ T cells and regulatory T cells, frequently co-expressed with PD-1. DNAM-1 expression was significantly reduced in tumors. However, contrasting pattern emerges with Tregs, which uniquely upregulate DNAM-1 in the PDAC TME. In addition, CD112 and CD155 were broadly expressed, including novel stromal CD112 localization. NK cells were nearly absent intratumorally, correlating with DNAM-1 downregulation.

conclusionsOur findings identify TIGIT as a promising immunotherapeutic target in PDAC and suggest that dual checkpoint blockade (TIGIT/PD-1), alongside restoration of DNAM-1 signaling, may overcome immune suppression. These results provide mechanistic rationale to inform future clinical trials in PDAC.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsReceptors, ImmunologicAntigens, Differentiation, T-LymphocyteB7-H1 AntigenBiomarkers, TumorCD8-Positive T-LymphocytesFemaleGene Expression Regulation, NeoplasticHumansLymphocytes, Tumor-InfiltratingMaleMiddle AgedProgrammed Cell Death 1 ReceptorReceptors, VirusT Lineage-Specific Activation Antigen 1Antigens, Differentiation, T-LymphocyteB7-H1 AntigenBiomarkers, TumorPDCD1 protein, humanpoliovirus receptorProgrammed Cell Death 1 ReceptorReceptors, ImmunologicReceptors, VirusTIGIT protein, humanT Lineage-Specific Activation Antigen 1Immune checkpointsPancreatic cancerTIGIT axisTumor immune microenvironment

Identifiers

PMID41805925
PMCPMC12976321

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.