ArticleOncoTargets and therapy2021
ILT4 in Colorectal Cancer Cells Induces Suppressive T Cell Contexture and Disease Progression.
Article in OncoTargets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Single-cell analysis reveals the prognostic role of immune escape in the colorectal cancer microenvironment.Translational cancer research · 2026Article
- Targeting leukocyte immunoglobulin‑like receptor B2 in the tumor microenvironment: A new treatment prospect for solid tumors (Review).Oncology letters · 2025Review
- Targeting ILT4 to Improve Immunotherapy Efficacy in Solid Tumour: From Bench to Bedside.ImmunoTargets and therapy · 2025Review
- LILRB2 promotes immune escape in breast cancer cells via enhanced HLA-A degradation.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- ILT4 facilitates angiogenesis in non-small cell lung cancer.Cancer science · 2024Article
- Analysis of HLA-G 14 bp Insertion/Deletion Polymorphism and HLA-G, ILT2 and ILT4 Expression in Head and Neck Squamous Cell Carcinoma Patients.Diseases (Basel, Switzerland) · 2024Article
- Targeting immune cell types of tumor microenvironment to overcome resistance to PD-1/PD-L1 blockade in lung cancer.Frontiers in pharmacology · 2023Review
- Review
- Tumor-derived immunoglobulin like transcript 5 induces suppressive immunocyte infiltration in colorectal cancer.Cancer science · 2022Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeImmune checkpoint blockade (ICB) therapy shows little or no clinical benefit in most colorectal cancer (CRC) patients, due to the immunosuppressive T cell contexture in the tumor microenvironment (TME). Immunoglobulin-like transcript (ILT) 4 is an immunosuppressive molecule in myeloid cells. ILT4 is enriched in solid tumor cells, facilitating their proliferation, invasion, and metastasis. However, the regulatory role of ILT4 in T cell immunity of CRC is still undetermined. Here, we aimed to explore how tumor cell-derived ILT4 orchestrates T cell infiltration, subset distribution, and function in CRC.
methodsA total of 145 paraffin-embedded cancer tissues and the corresponding clinicopathological information were collected from CRC patients. Immunohistochemical (IHC) staining and public database analyses determined the correlation of ILT4 expression with different T cell subset densities, IFN-γ levels, and patient outcomes. Paired Ig-like receptor B (PIR-B, ILT4 mouse ortholog)-overexpressing/-downregulated MC38 cells were subcutaneously injected into C57BL/6 mice as a CRC transplantation model. The frequencies, subsets, and IFN-γ levels of T cells in mouse blood and spleens were determined using flow cytometry and immunohistochemistry, respectively.
resultsHigh ILT4 expression in CRC cells was associated with decreased T cell infiltration, disease progression, and poor patient survival. T cell subset analyses indicated that ILT4-high patients showed reduced CD8
conclusionILT4 in CRC cells induced immunosuppressive T cell subset infiltration and impaired IFN-γ production in TILs, suggesting that ILT4 might be a potential immunotherapeutic target and prognostic biomarker.
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