AIM2 in tregs restrains anti-PD-1 efficacy by reinforcing immune suppression in MC38 colorectal cancer.

Nuo Wang, Hongwei Jiang, Zhang Fang, Jiajin Ma, Hui Ma, Bin Xu, Lujun Chen, Shaoxian Wu, Xiao Zheng

Abstract read

In one paragraph

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

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5 · Who and what money

Authors and funding

9 authors.

Nuo WangDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213003, China.

Hongwei JiangDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213003, China.

Zhang FangDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213003, China.

Jiajin MaDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213003, China.

Hui MaDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213003, China.

Bin XuDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213003, China.

Lujun ChenDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213003, China.

Shaoxian WuDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213003, China.

Xiao ZhengDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213003, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulatory T cells (Tregs) maintain immune homeostasis but also constrain antitumor immunity. Here, we show that the DNA sensor AIM2 sustains immunosuppressive programs in Tregs and limits responses to immune checkpoint blockade. Using an MC38 colorectal cancer model, Treg specific deletion of AIM2 enhanced the efficacy of PD1 blockade. This effect was associated with reduced effector Tregs and immunosuppressive myeloid populations, alongside increased cytotoxic activity of CD8 T cells. AIM2 deficient Tregs exhibited diminished suppressive programs and enhanced interferon responsive signatures, accompanied by broad remodeling of tumor immune interactions. These findings identify AIM2 as a key regulator of Treg mediated immune suppression and suggest that targeting AIM2 may improve the efficacy of cancer immunotherapy.

Indexed as

AIM2immune checkpoint inhibitorregulatory T cellstumor microenvironment

Identifiers

PMID42835088

DOI10.1016/j.isci.2026.116082

PMCPMC13634901

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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.