---
title: "ILDR2 promotes tumor immune evasion by recruiting CCR2+ monocytes in SCCVII tumors"
id: "pubmed-42323923"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42323923"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42323923/"
doi: "10.1016/j.bbrc.2026.154178"
published_at: "2026-09-03T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# ILDR2 promotes tumor immune evasion by recruiting CCR2+ monocytes in SCCVII tumors
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42323923
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42323923/)
- **DOI:** [10.1016/j.bbrc.2026.154178](https://doi.org/10.1016%2Fj.bbrc.2026.154178)
- **Published At:** 2026-09-03T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- B7 family co-inhibitory molecules regulate immune homeostasis but can suppress antitumor responses; **ILDR2** is a B7 family member that modulates T cell activation. - Prior work showed ILDR2 blockade can synergize with PD-L1 inhibition in mouse tumor models; the precise mechanism of ILDR2-mediated immune evasion was previously unclear. - The study used a mouse squamous cell carcinoma model (SCCVII) engineered to express the extracellular and transmembrane domains of **ILDR2** (ILDR2-SCCVII) and compared these to vector controls (Cont-SCCVII). - ILDR2-expressing tumors grew faster and, by day 21 after inoculation, had a lower proportion of activated T cells in the tumor microenvironment (**TME**) compared with controls. - At the late time point (day 21), most tumor-infiltrating leukocytes were **Ly6C- F4/80+ CD206+ M2-like macrophages**, consistent with an immunosuppressive, M2-polarized myeloid population. - At an earlier time point, ILDR2-SCCVII tumors showed increased infiltration of **Ly6C+ F4/80-/+ monocytes**, which are potential macrophage precursors. - Although tumor CCL2 expression rose early after inoculation in both groups, the receptor **CCR2** was more highly expressed on Ly6C+ monocytes specifically in ILDR2-expressing tumors. - Early recruited myeloid cells preferentially expressed **ILDR2** and bound ILDR2-Ig in assays using an in-house anti-mILDR2 monoclonal antibody and ILDR2-Ig, suggesting direct interaction between tumor-expressed ILDR2 and myeloid cells. - The authors propose that tumor ILDR2 promotes premature accumulation of CCR2+ monocytes via the **CCL2–CCR2 axis**, favoring subsequent M2 macrophage differentiation and an immunosuppressive TME that accelerates tumor growth. - Study context: experiments were performed in mice (SCCVII model, C57BL inbred background indicated in MeSH) and focused on myeloid cell dynamics and T cell activation; full experimental details and quantitative results are in the full text and not provided in the PubMed abstract.
## Clinical Analysis & Structured Key Points
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Epub 2026 Jun 20. # ILDR2 impairs antitumor surveillance by recruiting immunosuppressive CCR2+ monocytes [Yuto Nagatomo](https://pubmed.ncbi.nlm.nih.gov/?term=Nagatomo+Y&cauthor_id=42323923)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42323923/#full-view-affiliation-1 "Department of Molecular Immunology \(currently Department of Oral Biology\), Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Japan."), [Chenyang Zhang](https://pubmed.ncbi.nlm.nih.gov/?term=Zhang+C&cauthor_id=42323923)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42323923/#full-view-affiliation-1 "Department of Molecular Immunology \(currently Department of Oral Biology\), Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Japan."), [Yi Lu](https://pubmed.ncbi.nlm.nih.gov/?term=Lu+Y&cauthor_id=42323923)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42323923/#full-view-affiliation-1 "Department of Molecular Immunology \(currently Department of Oral Biology\), Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Japan."), [Amrita Widyagarini](https://pubmed.ncbi.nlm.nih.gov/?term=Widyagarini+A&cauthor_id=42323923)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42323923/#full-view-affiliation-1 "Department of Molecular Immunology \(currently Department of Oral Biology\), Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Japan."), [Shigenori Nagai](https://pubmed.ncbi.nlm.nih.gov/?term=Nagai+S&cauthor_id=42323923)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42323923/#full-view-affiliation-2 "Department of Molecular Immunology \(currently Department of Oral Biology\), Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Japan; Laboratory of Microbiology, Department of Food Science and Biotechnology, School of Food and Nutritional Sciences, Graduate School of Integrated Pharmaceutical and Nutritional Sciences, University of Shizuoka, Shizuoka, 422-8526, Japan. Electronic address: shigenagai@u-shizuoka-ken.ac.jp.") Affiliations Expand ### Affiliations * 1 Department of Molecular Immunology (currently Department of Oral Biology), Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Japan. * 2 Department of Molecular Immunology (currently Department of Oral Biology), Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Japan; Laboratory of Microbiology, Department of Food Science and Biotechnology, School of Food and Nutritional Sciences, Graduate School of Integrated Pharmaceutical and Nutritional Sciences, University of Shizuoka, Shizuoka, 422-8526, Japan. Electronic address: shigenagai@u-shizuoka-ken.ac.jp. * PMID: **42323923** * DOI: [ 10.1016/j.bbrc.2026.154178 ](https://doi.org/10.1016/j.bbrc.2026.154178) Item in Clipboard # ILDR2 impairs antitumor surveillance by recruiting immunosuppressive CCR2+ monocytes Yuto Nagatomo et al. Biochem Biophys Res Commun. 2026. Show details Display options Display options Format Abstract PubMed PMID Biochem Biophys Res Commun Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Biochem+Biophys+Res+Commun%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Biochem+Biophys+Res+Commun%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42323923/) . 2026 Sep 3:829:154178. doi: 10.1016/j.bbrc.2026.154178. Epub 2026 Jun 20. ### Authors [Yuto Nagatomo](https://pubmed.ncbi.nlm.nih.gov/?term=Nagatomo+Y&cauthor_id=42323923)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42323923/#short-view-affiliation-1 "Department of Molecular Immunology \(currently Department of Oral Biology\), Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Japan."), [Chenyang Zhang](https://pubmed.ncbi.nlm.nih.gov/?term=Zhang+C&cauthor_id=42323923)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42323923/#short-view-affiliation-1 "Department of Molecular Immunology \(currently Department of Oral Biology\), Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Japan."), [Yi Lu](https://pubmed.ncbi.nlm.nih.gov/?term=Lu+Y&cauthor_id=42323923)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42323923/#short-view-affiliation-1 "Department of Molecular Immunology \(currently Department of Oral Biology\), Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Japan."), [Amrita Widyagarini](https://pubmed.ncbi.nlm.nih.gov/?term=Widyagarini+A&cauthor_id=42323923)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42323923/#short-view-affiliation-1 "Department of Molecular Immunology \(currently Department of Oral Biology\), Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Japan."), [Shigenori Nagai](https://pubmed.ncbi.nlm.nih.gov/?term=Nagai+S&cauthor_id=42323923)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42323923/#short-view-affiliation-2 "Department of Molecular Immunology \(currently Department of Oral Biology\), Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Japan; Laboratory of Microbiology, Department of Food Science and Biotechnology, School of Food and Nutritional Sciences, Graduate School of Integrated Pharmaceutical and Nutritional Sciences, University of Shizuoka, Shizuoka, 422-8526, Japan. Electronic address: shigenagai@u-shizuoka-ken.ac.jp.") ### Affiliations * 1 Department of Molecular Immunology (currently Department of Oral Biology), Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Japan. * 2 Department of Molecular Immunology (currently Department of Oral Biology), Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Japan; Laboratory of Microbiology, Department of Food Science and Biotechnology, School of Food and Nutritional Sciences, Graduate School of Integrated Pharmaceutical and Nutritional Sciences, University of Shizuoka, Shizuoka, 422-8526, Japan. Electronic address: shigenagai@u-shizuoka-ken.ac.jp. * PMID: **42323923** * DOI: [ 10.1016/j.bbrc.2026.154178 ](https://doi.org/10.1016/j.bbrc.2026.154178) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract B7 family co-inhibitory molecules play a crucial role in maintaining homeostasis and preventing chronic inflammation. However, they also impede antitumor immune responses. Immunoglobulin-like domain-containing receptor 2 (ILDR2) is a B7 family member that modulates T cell activation. Previous studies demonstrated that its blockade synergizes with PD-L1 inhibition in mouse tumor models. Although ILDR2 likely contributes to immune evasion, the precise underlying mechanism remains unknown. Here, we investigated the effect of ILDR2 on the tumor microenvironment (TME) in a mouse squamous cell carcinoma (SCCVII) model. We generated ILDR2-expressing SCCVII cells (ILDR2-SCCVII) through transduction of the extracellular and transmembrane domains of ILDR2. Compared to control vector-transduced cells (Cont-SCCVII), ILDR2-SCCVII cells resulted in accelerated tumor growth and a reduced ratio of activated T cells in the TME 21 days after inoculation. At this late stage, most tumor-infiltrating leukocytes were Ly6C- F4/80+ CD206+ M2-like macrophages. Interestingly, at an earlier time point, we observed the increased infiltration of Ly6C+ F4/80-/+ monocytes-potential macrophage precursors-in ILDR2-SCCVII tumors. Whereas CCL2 expression was enhanced early after inoculation in both groups, its receptor CCR2 was more highly expressed on Ly6C+ F4/80-/+ monocytes specifically in the ILDR2-SCCVII group. Using our in-house anti-mILDR2 monoclonal antibody and ILDR2-Ig, we found that early recruited myeloid cells preferentially expressed ILDR2 and exhibited ILDR2-Ig binding. These results suggest that tumor-expressing ILDR2 interacts with myeloid cells during the early stages of tumor development, inducing premature monocyte accumulation via the CCL2-CCR2 axis. This early shift toward an M2 macrophage-mediated immunosuppressive environment likely accelerates tumor growth. **Keywords:** CCL2–CCR2 axis; Immunoglobulin-like domain-containing receptor-2 (ILDR2); M2 macrophage; Monocyte; Squamous cell carcinoma (SCCVII); Tumor microenvironment (TME). Copyright © 2026 Elsevier Inc. All rights reserved. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declaration of competing interest The authors declare that they have no known competing financial interest or personal relationships that could have appeared to influence the work reported in this paper. ## Similar articles * [ B7-H3 Suppresses Antitumor Immunity via the CCL2-CCR2-M2 Macrophage Axis and Contributes to Ovarian Cancer Progression. ](https://pubmed.ncbi.nlm.nih.gov/34799346/) Miyamoto T, Murakami R, Hamanishi J, Tanigaki K, Hosoe Y, Mise N, Takamatsu S, Mise Y, Ukita M, Taki M, Yamanoi K, Horikawa N, Abiko K, Yamaguchi K, Baba T, Matsumura N, Mandai M.Miyamoto T, et al.Cancer Immunol Res. 2022 Jan;10(1):56-69. doi: 10.1158/2326-6066.CIR-21-0407. Epub 2021 Nov 19.Cancer Immunol Res. 2022.PMID: 34799346Free PMC article. * [ Sublingual macrophage-associated ILDR2 contributes to immune tolerance via Treg induction. ](https://pubmed.ncbi.nlm.nih.gov/39626366/) Sultana F, Widyagarini A, Kawano Y, Ohsugi Y, Katagiri S, Azuma M, Nagai S.Sultana F, et al.Biochem Biophys Res Commun. 2025 Jan;742:151009. doi: 10.1016/j.bbrc.2024.151009. Epub 2024 Nov 15.Biochem Biophys Res Commun. 2025.PMID: 39626366 * [ ILT4 inhibition prevents TAM- and dysfunctional T cell-mediated immunosuppression and enhances the efficacy of anti-PD-L1 therapy in NSCLC with EGFR activation. ](https://pubmed.ncbi.nlm.nih.gov/33537094/) Chen X, Gao A, Zhang F, Yang Z, Wang S, Fang Y, Li J, Wang J, Shi W, Wang L, Zheng Y, Sun Y.Chen X, et al.Theranostics. 2021 Jan 19;11(7):3392-3416. doi: 10.7150/thno.52435. eCollection 2021.Theranostics. 2021.PMID: 33537094Free PMC article. * [ Tumor cell-released autophagosomes (TRAPs) promote immunosuppression through induction of M2-like macrophages with increased expression of PD-L1. ](https://pubmed.ncbi.nlm.nih.gov/30563569/) Wen ZF, Liu H, Gao R, Zhou M, Ma J, Zhang Y, Zhao J, Chen Y, Zhang T, Huang F, Pan N, Zhang J, Fox BA, Hu HM, Wang LX.Wen ZF, et al.J Immunother Cancer. 2018 Dec 18;6(1):151. doi: 10.1186/s40425-018-0452-5.J Immunother Cancer. 2018.PMID: 30563569Free PMC article. * [ Targeting the CCL2/CCR2 Axis in Cancer Immunotherapy: One Stone, Three Birds? ](https://pubmed.ncbi.nlm.nih.gov/34804061/) Fei L, Ren X, Yu H, Zhan Y.Fei L, et al.Front Immunol. 2021 Nov 3;12:771210. doi: 10.3389/fimmu.2021.771210. eCollection 2021.Front Immunol. 2021.PMID: 34804061Free PMC article.Review. 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