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作者

Jiaxin Yin, Yuxiao Song, Yang Fu, Jun Wang, Zhimin Zhang, Shasha Ruan, Gaoli Liu, Bicheng Zhang

作者单位

Affiliations ¹ Cancer Center, Renmin Hospital of Wuhan University, Wuhan, China. ² Department of Oncology, Xiangyang Hospital, Hubei University of Chinese Medicine, Xiangyang, China. ³ Department of Oncology, The First Affiliated Hospital of Shandong First Medical University, Jinan, China. ⁴ Department of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan, China. ⁵ Cancer Center, Renmin Hospital of Wuhan University, Wuhan, China. bichengzhang@hotmail.com.

刊名

Cancer immunology, immunotherapy : CII

年份

2024

卷号

Vol.74 No.1

页码

16

ISSN

1432-0851

关键词

C1qA LILRB4 Lung adenocarcinoma NF-κB NLRP12 Tumor-associated macrophages.

摘要

The anti-tumor immune response is greatly hindered by the protumor polarization of tumor-associated macrophages . Cancer-related inflammation plays a central role in TAMs protumor polarization. Our study explored the unique positive feedback loop between inflammasome and complement in TAMs. The present study identified NOD-like receptors family pyrin domain containing 12 formed positive feedback with C1qA and drove TAMs protumor polarization via the LILRB4/NF-κB pathway. In addition, NLRP12 was...更多

The anti-tumor immune response is greatly hindered by the protumor polarization of tumor-associated macrophages . Cancer-related inflammation plays a central role in TAMs protumor polarization. Our study explored the unique positive feedback loop between inflammasome and complement in TAMs. The present study identified NOD-like receptors family pyrin domain containing 12 formed positive feedback with C1qA and drove TAMs protumor polarization via the LILRB4/NF-κB pathway. In addition, NLRP12 was predominantly expressed in TAMs and was associated with poorer prognosis in lung adenocarcinoma patients. Knocking down LILRB4 inhibited TAMs protumor polarization. NLRP12-overexpressing TAMs promoted tumor cells' malignant progression and inhibited T cells' proliferation and cytotoxic function. Lastly, NLRP12 knockout reversed macrophage polarization, enhanced T-cell anti-tumor immunity, and suppressed tumor growth. Our findings highlighted the essential role of NLRP12/C1qA positive feedback loop and the LILRB4/NF-κB pathway in promoting TAMs protumor polarization. Inhibition of NLRP12 suppressed tumor development and promoted immune response. NLRP12 may be a promising target for LUAD immunotherapy.收起

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