Evidence map›Paper›PMID 42527663›Full record

ArticleCellular & molecular immunology2026

NLRC3 enhances antitumor immunity by specifically negatively regulating M-MDSCs in a STING-dependent manner.

Yuling Fu, Xiaoxia Zhan, Shousheng Liu, Qinhan Xie, Shijie Song, Suwan Wu, Junli Sheng, Huiru He, Xiaolong You, Qiao Ling and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular & molecular immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

17 authors.

Yuling Fu *Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Xiaoxia Zhan *Department of Laboratory Medicine, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Shousheng Liu *Department of General Medicine, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou, China.
Qinhan XieGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Shijie SongGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Suwan WuGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Junli ShengGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Huiru HeGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Xiaolong YouGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Qiao LingGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Xiaodan YangGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Zulaya AbudureyimuGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Wenhao LuGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Wen LiGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Jia TangNHC Key Laboratory of Male Reproduction and Genetics, Guangdong Provincial Reproductive Science Institute (Guangdong Provincial Fertility Hospital), Guangzhou, Guangdong, China. tangjia@jnu.edu.cn.
Peng WangDepartment of Emergency Medicine, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China. wangp49@mail.sysu.edu.cn.
Shengfeng HuGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China. hushengfeng@gzhmu.edu.cn.ORCID 0000-0001-7901-4410

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82270600National Natural Science Foundation of China (National Science Foundation of China) 82272239National Natural Science Foundation of China (National Science Foundation of China) 82471780
6 · The paper itself

Abstract

NOD-like receptor (NLR) family CARD domain containing 3 (NLRC3), an intracellular member of the NLR family, is a negative regulator of both immune cell modulation and tumor cell proliferation. However, the role of NLRC3 and the mechanisms underlying its effect on the tumor immune microenvironment remain unclear. In this study, we report that NLRC3 promotes antitumor immunity by specifically negatively regulating the infiltration and immunosuppressive function of monocytic myeloid-derived suppressor cells (M-MDSCs). Mechanistically, NLRC3 inhibits the stimulator of interferon genes (STING) signaling pathway, leading to reduced expression of programmed cell death ligand 1 (PD-L1) and CCR2 in M-MDSCs, thereby limiting the infiltration and immunosuppressive function of M-MDSCs. Notably, overexpression of NLRC3 in combination with the STING agonist c-GAMP significantly inhibited tumor growth. These findings reveal a critical role for NLRC3 in modulating the immune microenvironment and provide insights into the optimization of NLRC3-targeted therapeutics.

Indexed as

Membrane ProteinsMyeloid-Derived Suppressor CellsAnimalsCell Line, TumorcGAS-STING Signaling PathwayHumansIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLReceptors, CCR2Signal TransductionSTING ProteinTumor MicroenvironmentCcr2 protein, mouseIntercellular Signaling Peptides and ProteinsMembrane ProteinsNLRC3 protein, mouseReceptors, CCR2Sting1 protein, mouseSTING ProteinCCR2M-MDSCNLRC3PD-L1STING

Identifiers

PMID42527663
PMCPMC13526779

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.