NLRP3炎性小体与MDSC在骨髓增生异常综合征中的作用及研究进展
The Role and Research Progress of NLRP3 Inflammasome and MDSC in Myelodysplastic Syndrome
DOI: 10.12677/ACM.2023.133564, PDF,   
作者: 张晓华, 郝建萍*：新疆医科大学第一附属医院血液病中心，新疆 乌鲁木齐
关键词: NLRP3炎症小体；髓源性抑制细胞；骨髓增生异常综合征；NLRP3 Inflammasome； Myeloid Derived Suppressor Cells； Myelodysplastic Syndrome
摘要: NLRP3炎症小体是近年来研究较为深入的炎症复合体之一，其不仅在各种炎性疾病中发挥重要作用，而且与肿瘤的发生发展有密切关系。髓源性抑制细胞(MDSCs)是肿瘤微环境的主要组成部分，有强大的免疫抑制活性，在肿瘤、感染和炎症中可异常增多，有效抑制T细胞、B细胞对肿瘤的杀伤，与骨髓增生异常综合征(MDS)的发生发展密切相关。最新研究表明，NLRP3炎症小体的效应因子IL-1β可招募大量的髓源性抑制细胞(MDSCs)到肿瘤部位，协助肿瘤细胞逃避免疫监测，促进肿瘤的发展。本文就NLRP3炎症小体与MDSC在MDS发病过程中的作用及研究进展作一综述。
Abstract: NLRP3 inflammasome are one of the inflammatory complexes that have been intensively studied in recent years. They not only play an important role in various inflammatory diseases, but also have a close relationship with the occurrence and development of tumors. Myeloid-derived suppressor cells (MDSCs) are the main components of tumor microenvironment. They have strong immunosuppressive activity and can increase abnormally in tumor, infection and inflammation. They can effectively inhibit the killing of tumor by T cells and B cells, and are closely related to the occurrence and development of myelodysplastic syndrome (MDS). Recent studies have shown that IL-1β, an effector of NLRP3 inflammatory vesicles, recruits large numbers of myeloid-derived sup-pressor cells (MDSCs) to tumour sites, assisting tumour cells to evade immune surveillance and promoting tumour progression. This article reviews the role and research progress of NLRP3 inflammasome and MDSC in the pathogenesis of MDS.
文章引用：张晓华, 郝建萍. NLRP3炎性小体与MDSC在骨髓增生异常综合征中的作用及研究进展[J]. 临床医学进展, 2023, 13(3): 3932-3936. https://doi.org/10.12677/ACM.2023.133564

参考文献

[1] Hemenway, G. and Frishman, W.H. (2022) Therapeutic Implications of NLRP3-Mediated Inflammation in Coronary Artery Disease. Cardiology in Review, 30, 90-99. [Google Scholar] [CrossRef] 
[2] Lee, H.E., Lee, J.Y., Yang, G., et al. (2019) Inhibition of NLRP3 Inflammasome in Tumor Microenvironment Leads to Suppression of Metastatic Potential of Cancer Cells. Scientific Reports, 9, Article No. 12277. [Google Scholar] [CrossRef] [PubMed]
[3] Wang Z, Zhang S, Xiao Y, et al. (2020) NLRP3 Inflammasome and Inflammatory Diseases. Oxidative Medicine and Cellular Longevity, 2020, Article ID: 4063562. [Google Scholar] [CrossRef] [PubMed]
[4] Liu, D., Zeng, X., Li, X., et al. (2020) Advances in the Molecular Mechanisms
of NLRP3 Inflammasome Activators and Inactivators. Biochemical Pharmacology, 175, Article ID: 113863. [Google Scholar] [CrossRef] [PubMed]
[5] Zhang, B., Wei, W. and Qiu, J. (2018) ALK Is Required for NLRP3 Inflammasome Activation in Macrophage. Biochemical and Biophysical Research Communications, 501, 246-252. [Google Scholar] [CrossRef] [PubMed]
[6] Kelley, N., Jeltema, D., Duan, Y., et al. (2019) The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation. International Journal of Molecular Sciences, 20, 3328. [Google Scholar] [CrossRef] [PubMed]
[7] 杨斯迪, 邓奇峰, 黄瑞, 吴淑燕. 炎性小体激活与细胞焦亡的研究进展[J]. 微生物与感染, 2017, 12(3): 192-196.
[8] 肖少波, 等. 细胞焦亡: 一种与炎症相关的细胞死亡[J]. 生命的化学, 2017, 37(3): 423-428.
[9] 刘超英, 等. 细胞焦亡与炎症发生研究进展[J]. 动物医学进展, 2017, 38(9): 101-104.
[10] 黄茂凌, 等. 细胞焦亡发生机制及其与相关疾病的研究进展[J]. 疑难病杂志, 2019, 18(7): 744-747.
[11] 祁会丽, 等. 细胞焦亡激活机制及相关疾病研究进展[J]. 中华实用诊断与治疗杂志, 2016, 30(5): 417-419.
[12] Yang, J., Zhao, Y. and Feng, S. (2015) Non-Canonical Activation of Inflammatory Caspases by Cytosolic LPS in Innate Immunity. Current Opinion in Immunology, 32, 78-83. [Google Scholar] [CrossRef] [PubMed]
[13] Cazzola, M. (2020) Myelodysplastic Syndromes. New England Journal of Medicine, 383, 1358-1374. [Google Scholar] [CrossRef] 
[14] Basiorka, A.A., McGraw, K.L., Eksioglu, E.A., et al. (2016) The NLRP3
Inflammasome Functions as a Driver of the Myelodysplastic Syndrome Phenotype. Blood, 128, 2960-2975. [Google Scholar] [CrossRef] [PubMed]
[15] 王金霞, 刘爱飞, 李方林, 陈懿建. 炎症小体在恶性血液病发病中的作用[J]. 中国老年学杂志, 2017, 37(16): 4154-4156.
[16] Sallman, D.A., Cluzeau, T., Basiorka, A.A., et al. (2016) Unraveling the Pathogenesis of MDS: The NLRP3 Inflammasome and Pyroptosis Drive the MDS Pheno-Type U. Frontiers in Oncology, 6, 151. [Google Scholar] [CrossRef] [PubMed]
[17] Zhong, C., Wang, R., Hua, M., et al. (2021) NLRP3 Inflammasome Promotes the Progression of Acute Myeloid Leukemia via IL-1β Pathway. Frontiers in Immunology, 12, 2113. [Google Scholar] [CrossRef] [PubMed]
[18] Sallman, D.A. and List, A. (2019) The Central Role of Inflam-matory Signaling in
the Pathogenesis of Myelodysplastic Syndromes. Blood, 133, 1039-1048. [Google Scholar] [CrossRef] [PubMed]
[19] Fleming, V., Hu, X., Weber, R., et al. (2018) Targeting My-eloid-Derived Suppressor Cells to Bypass Tumor-Induced Immunosuppression. Frontiers in Immunology, 9, 98. [Google Scholar] [CrossRef] [PubMed]
[20] Ehsan, N., Ali, M., Mohammad, S.P., et al. (2021) Role of Mye-loid-Derived Suppressor Cell (MDSC) in Autoimmunity and Its Potential as a Therapeutic Target. Inflammopharmacology, 29, 1307-1315. [Google Scholar] [CrossRef] [PubMed]
[21] Li, L.H., Yu, R., Cai, T.G., et al. (2020) Effects of Immune Cells and Cytokines on Inflammation and Immunosuppression in the Tumor Microenvironment. International Immunopharmacology, 88, Article ID: 106939. [Google Scholar] [CrossRef] [PubMed]
[22] Barreyro, L., Chlon, T.M. and Starczynowski, D.T. (2018) Chronic Immune Response Dysregulation in MDS Pathogenesis. Blood, 132, 1553-1560. [Google Scholar] [CrossRef] [PubMed]
[23] Qi, X., Jiang, H.J. Liu, P., et al. (2021) Increased Mye-loid-Derived Suppressor Cells in Patients with Myelodysplastic Syndromes Suppress CD8+ T Lymphocyte Function through the STAT3-ARG1 Pathway. Leukemia & Lymphoma, 62, 218-223. [Google Scholar] [CrossRef] [PubMed]
[24] Braun, T., Carvalho, G., Coquelle, A., et al. (2006) NF-kappaB Constitutes a Potential Therapeutic Target
in High-Risk Myelodysplastic Syndrome. Blood, 107, 1156-1165. [Google Scholar] [CrossRef] [PubMed]
[25] Han, D., Tao, J., Fu, R., et al. (2020) Myeloid-Derived Suppressor Cell Cytokine Secretion as Prognostic Factor in Myelodysplastic Syndromes. Innate Immunity, 26, 703-715. [Google Scholar] [CrossRef] [PubMed]
[26] Ben-Neriah, Y. and Karin, M. (2011) Inflammation Meets Cancer, with NF-KB as the Matchmaker. Nature Immunology, 12, 715-723. [Google Scholar] [CrossRef] [PubMed]
[27] Sallman, D.A., Tanaka, T.N., List, A., et al. (2017) SOHO State of the Art
Update and Next Questions: Biology and Treatment of Myelodysplastic Syndromes. Clinical Lymphoma, Myeloma and Leukemia, 17, 613-620. [Google Scholar] [CrossRef] [PubMed]
[28] Ward, G.A., McGraw, K.L., Abbas-Aghabababababababeh, F., et al. (2021) Oxidized Mitochondrial DNA Released after Inflammasome Activation Is a Disease Biomarker for Myelodysplastic Syndromes. Blood Advances, 5, 2216-2228. [Google Scholar] [CrossRef] [PubMed]
[29] Chen, L., Huang, C.F., Li, Y.C., et al. (2018) Blockage of the NLRP3 Inflammasome by MCC950 Improves Anti-Tumor Immune Responses in Head and Neck Squamous Cell Carcinoma. Cellular and Molecular Life Sciences, 75, 2045-2058. [Google Scholar] [CrossRef] [PubMed]
[30] Shi, H., Qin, Y., Tian, Y., et al. (2022) Interleukin-1beta Triggers the Expansion of Circulating Granulocytic Myeloid-Derived Suppressor Cell Subset Dependent on Erk 1/2 Activation. Immunobiology, 227, 152-165. [Google Scholar] [CrossRef] [PubMed]
[31] Tu, S., Bhagat, G., Cui, G., et al. (2008) Overexpression of In-terleukin-1β Induces Gastric Inflammation and Cancer and Mobilizes Myeloid-Derived Suppressor Cells in Mice. Cancer Cell, 14, 408-419. [Google Scholar] [CrossRef] [PubMed]

为你推荐