Evidence map›Paper›PMID 41117057›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

MARCO+ Tumor-Associated Macrophages Impede CD8+ T Cell Immunity to Facilitate Immunotherapy Resistance in Renal Cell Carcinoma.

Jiayuan Chen, Jiazhi Mo, Jinchang Wei, Mengnan Qu, Jie Dai, Yan Kong, Huayan Xu, Juan Li, Xieqiao Yan, Chuanliang Cui and 5 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
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

15 authors.

Jiayuan ChenDepartment of Genitourinary Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Peking University, Beijing, 100142, China.
Jiazhi MoDepartment of Genitourinary Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Peking University, Beijing, 100142, China.
Jinchang WeiDepartment of Genitourinary Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Peking University, Beijing, 100142, China.
Mengnan QuDepartment of Genitourinary Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Peking University, Beijing, 100142, China.
Jie DaiDepartment of Melanoma and Sarcoma, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Peking University, Beijing, 100142, China.
Yan KongDepartment of Melanoma and Sarcoma, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Peking University, Beijing, 100142, China.
Huayan XuDepartment of Genitourinary Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Peking University, Beijing, 100142, China.
Juan LiDepartment of Genitourinary Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Peking University, Beijing, 100142, China.
Xieqiao YanDepartment of Genitourinary Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Peking University, Beijing, 100142, China.
Chuanliang CuiDepartment of Genitourinary Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Peking University, Beijing, 100142, China.
Lu SiDepartment of Melanoma and Sarcoma, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Peking University, Beijing, 100142, China.
Zhihong ChiDepartment of Melanoma and Sarcoma, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Peking University, Beijing, 100142, China.
Jun GuoDepartment of Genitourinary Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Peking University, Beijing, 100142, China.
Xiaowen WuDepartment of Genitourinary Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Peking University, Beijing, 100142, China.
Xinan ShengDepartment of Genitourinary Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Peking University, Beijing, 100142, China.ORCID https://orcid.org/0000-0001-9359-0975

Funding

Beijing Natural Science Foundation L244024Education Ministry's Chunhui Program Cooperative Research Project HZKY20220029Natural Science Foundation of China 82172604Natural Science Foundation of China 82473199
6 · The paper itself

Abstract

Immune checkpoint blockade (ICB) therapy, especially in combination regimens, has significantly increased survival of renal cell carcinoma (RCC) patients. However, the ICB-resistant mechanisms remain largely unclear and require further investigation. Here, an immunosuppressive ecosystem in ICB-resistant tumors is identified, featured by preferential infiltration of MARCO+ tumor-associated macrophages (TAMs) and restrained cytotoxicity of CD8+ cytotoxic T lymphocytes (CTLs). The infiltrated MARCO+ TAMs can obstruct the development of CD8+ CTLs by impairing MHC-I-mediated neoantigen cross-presentation. Mechanistically, MARCO up-regulates the expression of SOCS1, which obstructs the kinase activity of JAK1, thereby downregulating MHC-I expression through the inhibition of the JAK1-STAT1-NLRC5 signaling cascade. Further, MARCO blockade significantly facilitates ICB therapy in in vivo models by recovering tumor recognition and priming anti-tumor CD8+ T cell responses. Taken together, these findings highlight MARCO as a highly desirable target in ICB-refractory individuals for immunorecognition reignition and immunotherapy modulation.

Indexed as

Carcinoma, Renal CellCD8-Positive T-LymphocytesKidney NeoplasmsTumor-Associated MacrophagesAnimalsCell Line, TumorHumansImmune Checkpoint InhibitorsImmunotherapyMiceMice, Inbred C57BLTumor MicroenvironmentImmune Checkpoint InhibitorsimmunotherapymacrophagesMARCOrenal cell carcinomasingle‐cell RNA‐seq

Identifiers

PMID41117057
PMCPMC12713061

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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.