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NLR members in inflammation-associated carcinogenesis

Cellular & Molecular Immunology volume 14, pages 403–405 (2017)Cite this article

Chronic inflammation is regarded as an important factor in cancer progression. In addition to the immune surveillance function in the early stage of tumorigenesis, inflammation is also known as one of the hallmarks of cancer and can supply the tumor microenvironment with bioactive molecules and favor the development of other hallmarks of cancer, such as genetic instability and angiogenesis. Moreover, inflammation contributes to the changing tumor microenvironment by altering stromal cell turnover rates and polarizing immune cell immunosuppressive capabilities.1 In addition, many tumor suppressor genes have been reported to be involved in inflammation modulation.2 However, the types of molecules and the underlying mechanisms involved in inflammation-associated cancer need to be further investigated, which may provide new targets for the control of cancer.

Recognition of danger-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs) is the key step that modulates inflammation. Five major PRR families have been reported to be involved in tumorigenesis, including the Toll-like receptors (TLRs), C-type lectin receptors (CLRs), RIG-I-like receptors (RLRs), absent-in-melanoma (AIM)-like receptors (ALRs) and the nucleotide-binding and oligomerization domain (NOD)-like receptors (NLRs). TLRs and CLRs are located in the plasma membranes, whereas RLRs, ALRs and NLRs are intracellular PRRs.3 Unlike other families that have been shown to bind their specific cognate ligands, the distinct ligands for NLRs are still unknown. In fact, mounting evidence suggests that NLRs function as cytoplasmic sensors and participate in modulating TLR, RLR and CLR signaling pathways.4 NLRs can sense stimulatory signals from pathogens, host cells and environmental sources, although the interaction patterns are still unclear.3 Importantly, dysfunction of NLRs leads to various inflammatory diseases, autoimmune diseases and inflammation-associated carcinogenesis.5 Given the vital roles of NLRs in inflammation and disease progression, research is now focused on elucidating their roles in the pathogenesis of diseases such as cancer, with the aim of finding new therapeutic targets.

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Authors and Affiliations

  1. Institute of Immunology, Zhejiang University School of Medicine, Hangzhou, 310058, China

    Ha Zhu & Xuetao Cao

  2. National Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, 200433, China

    Ha Zhu & Xuetao Cao

  3. Department of Immunology & Center for Immunotherapy, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, 100005, China

    Xuetao Cao

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Correspondence to Xuetao Cao.

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Zhu, H., Cao, X. NLR members in inflammation-associated carcinogenesis. Cell Mol Immunol 14, 403–405 (2017). https://doi.org/10.1038/cmi.2017.14

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