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本文引用的文献

1
Inhibition of Bruton tyrosine kinase in patients with severe COVID-19.在重症 COVID-19 患者中抑制布鲁顿酪氨酸激酶。
Sci Immunol. 2020 Jun 5;5(48). doi: 10.1126/sciimmunol.abd0110.
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The pathogenicity of SARS-CoV-2 in hACE2 transgenic mice.严重急性呼吸综合征冠状病毒2(SARS-CoV-2)在人血管紧张素转换酶2(hACE2)转基因小鼠中的致病性。
Nature. 2020 Jul;583(7818):830-833. doi: 10.1038/s41586-020-2312-y. Epub 2020 May 7.
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Pathological inflammation in patients with COVID-19: a key role for monocytes and macrophages.COVID-19 患者的病理性炎症:单核细胞和巨噬细胞的关键作用。
Nat Rev Immunol. 2020 Jun;20(6):355-362. doi: 10.1038/s41577-020-0331-4. Epub 2020 May 6.
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SARS-CoV-2 entry factors are highly expressed in nasal epithelial cells together with innate immune genes.严重急性呼吸综合征冠状病毒2(SARS-CoV-2)进入因子与固有免疫基因一起在鼻上皮细胞中高表达。
Nat Med. 2020 May;26(5):681-687. doi: 10.1038/s41591-020-0868-6. Epub 2020 Apr 23.
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The BTK inhibitor ibrutinib may protect against pulmonary injury in COVID-19-infected patients.布鲁顿酪氨酸激酶(BTK)抑制剂依鲁替尼可能对新冠病毒感染患者的肺损伤具有保护作用。
Blood. 2020 May 21;135(21):1912-1915. doi: 10.1182/blood.2020006288.
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Clinical and immunological features of severe and moderate coronavirus disease 2019.新型冠状病毒病 2019 重症和中度患者的临床和免疫学特征。
J Clin Invest. 2020 May 1;130(5):2620-2629. doi: 10.1172/JCI137244.
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Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China.中国武汉地区 2019 年新型冠状病毒感染患者的临床特征。
Lancet. 2020 Feb 15;395(10223):497-506. doi: 10.1016/S0140-6736(20)30183-5. Epub 2020 Jan 24.
8
Evidence for interaction of the NLRP3 inflammasome and Bruton's tyrosine kinase in tumor-associated macrophages: implications for myeloid cell production of interleukin-1beta.NLRP3炎性小体与布鲁顿酪氨酸激酶在肿瘤相关巨噬细胞中的相互作用证据:对髓样细胞产生白细胞介素-1β的影响
Oncoimmunology. 2019 Sep 5;8(11):1659704. doi: 10.1080/2162402X.2019.1659704. eCollection 2019.
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The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation.NLRP3 炎性小体:激活和调节机制概述。
Int J Mol Sci. 2019 Jul 6;20(13):3328. doi: 10.3390/ijms20133328.
10
Severe Acute Respiratory Syndrome Coronavirus Viroporin 3a Activates the NLRP3 Inflammasome.严重急性呼吸综合征冠状病毒病毒孔蛋白3a激活NLRP3炎性小体。
Front Microbiol. 2019 Jan 29;10:50. doi: 10.3389/fmicb.2019.00050. eCollection 2019.

观察布鲁顿酪氨酸激酶抑制剂在 SARS-CoV-2 和癌症中的应用。

Observations on the use of Bruton's tyrosine kinase inhibitors in SAR-CoV-2 and cancer.

机构信息

Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.

Department of Surgery, Division of Surgical Oncology, The Ohio State University, N924 Doan Hall, 410 W. 10th Ave, Columbus, OH, 43210, USA.

出版信息

J Hematol Oncol. 2021 Jan 13;14(1):15. doi: 10.1186/s13045-020-00999-8.

DOI:10.1186/s13045-020-00999-8
PMID:33441177
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7805262/
Abstract

Bruton's tyrosine kinase (BTK) inhibitors, drugs utilized in cancer, are being repurposed for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) (COVID-19). Recently, BTK inhibitors acalabrutinib and ibrutinib have been found to protect against pulmonary injury in a small group of patients infected with SARS-CoV-2. The high levels of pro-inflammatory cytokines found in the circulation of COVID-19 patients with severe lung disease suggest the involvement of the innate immune system in this process. Understanding the potential mechanism of action of BTK inhibition in SARS-CoV-2 is clearly of importance to determine how acalabrutinib, ibrutinib and possibly other BTK inhibitors may provide protection against lung injury.

摘要

布鲁顿酪氨酸激酶(BTK)抑制剂是用于癌症治疗的药物,现正被重新用于治疗严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)(COVID-19)。最近发现,BTK 抑制剂阿卡替尼和依鲁替尼可预防一小部分感染 SARS-CoV-2 的患者发生肺部损伤。COVID-19 患者发生严重肺部疾病时循环中发现的高水平促炎细胞因子表明,先天免疫系统在此过程中发挥作用。明确 BTK 抑制在 SARS-CoV-2 中的潜在作用机制对于确定阿卡替尼、依鲁替尼和可能的其他 BTK 抑制剂如何提供肺部损伤保护作用非常重要。