Evidence map›Paper›PMID 34277113›Full record

ArticleImmune network2021

Enriching CCL3 in the Tumor Microenvironment Facilitates T cell Responses and Improves the Efficacy of Anti-PD-1 Therapy.

Tae Gun Kang, Hyo Jin Park, Jihyun Moon, June Hyung Lee, Sang-Jun Ha

Open access · diamondAbstract read
In one paragraph

Article in Immune network, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

24 citing papers in PubMed, 26 citations in OpenAlex.

  1. Trial
  2. Unraveling CD4Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
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  16. Inflammatory factors collaboratively linkFrontiers in immunology · 2025
    Review
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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

5 authors at 2 institutions in 1 country.

Tae Gun KangDepartment of Biochemistry, College of Life Science & Biotechnology, Yonsei University, Seoul 03722, Korea.ORCID https://orcid.org/0000-0002-2997-9887
Hyo Jin ParkYuhan Corporation, Chemistry & Chemical Biology Team, Yuhan R&D Institute, Seoul 06927, Korea.ORCID https://orcid.org/0000-0003-4142-3862
Jihyun MoonDepartment of Biochemistry, College of Life Science & Biotechnology, Yonsei University, Seoul 03722, Korea.ORCID https://orcid.org/0000-0001-5323-4781
June Hyung LeeYuhan Corporation, Biologics Discovery Team, Seoul 06927, Korea.ORCID https://orcid.org/0000-0002-5841-5749
Sang-Jun HaDepartment of Biochemistry, College of Life Science & Biotechnology, Yonsei University, Seoul 03722, Korea.ORCID https://orcid.org/0000-0002-1192-6031
Yonsei University · KRYuhan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemokines are key factors that influence the migration and maintenance of relevant immune cells into an infected tissue or a tumor microenvironment. Therefore, it is believed that the controlled administration of chemokines in the tumor microenvironment may be an effective immunotherapy against cancer. Previous studies have shown that CCL3, also known as macrophage inflammatory protein 1-alpha, facilitates the recruitment of dendritic cells (DCs) for the presentation of tumor Ags and promotes T cell activation. Here, we investigated the role of CCL3 in regulating the tumor microenvironment using a syngeneic mouse tumor model. We observed that MC38 tumors overexpressing CCL3 (CCL3-OE) showed rapid regression compared with the wild type MC38 tumors. Additionally, these CCL3-OE tumors showed an increase in the proliferative and functional tumor-infiltrating T cells. Furthermore, PD-1 immune checkpoint blockade accelerated tumor regression in the CCL3-OE tumor microenvironment. Next, we generated a modified CCL3 protein for pre-clinical use by fusing recombinant CCL3 (rCCL3) with a non-cytolytic hybrid Fc (HyFc). Administering a controlled dose of rCCL3-HyFc via subcutaneous injections near tumors was effective in tumor regression and improved survival along with activated myeloid cells and augmented T cell responses. Furthermore, combination therapy of rCCL3-HyFc with PD-1 blockade exhibited prominent effect to tumor regression. Collectively, our findings demonstrate that appropriate concentrations of CCL3 in the tumor microenvironment would be an effective adjuvant to promote anti-tumor immune responses, and suggest that administering a long-lasting form of CCL3 in combination with PD-1 blockers can have clinical applications in cancer immunotherapy.

Indexed as

Chemokine CCL3Immune checkpoint blockadeImmunotherapyTumor microenvironment

Identifiers

PMID34277113
PMCPMC8263215
OpenAlexW3182169615

What OpenQuestion holds

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Registered trials

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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.