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血液系统恶性肿瘤中的CCL17、CCL22及其受体CCR4

CCL17, CCL22 and their receptor CCR4 in hematologic malignancies.

作者信息

Zou Shasha, Liu Bo, Feng Yonghuai

机构信息

Department of Hematology, Affiliated Hospital of Zunyi Medical University, Zunyi, China.

Department of Key, Lab for Basic Pharmacology and Joint International Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, China.

出版信息

Discov Oncol. 2024 Sep 6;15(1):412. doi: 10.1007/s12672-024-01210-x.

Abstract

Hematological malignancies (HM) are common malignant tumors with high morbidity and mortality rates, and are malignant diseases that seriously affect human health, with chemotherapy prone to recurrence and toxic side effects. Therefore, the development of precise, effective, and safe targeted therapeutic agents has become a hotspot in the current research of antitumor technology. More and more studies have shown that the interaction of C-C chemokine ligand 17 (CCL17) and C-C chemokine ligand 22 (CCL22) with the receptor C-C chemokine receptor type 4 (CCR4) promotes the immune escape of tumors and is closely related to the occurrence, development, and prognosis of hematological tumors. In this regard, we present a review on the expression and role of the CCL17/CCL22-CCR4 axis in HM, including lymphoma, leukemia, and multiple myeloma, with the aim of providing latest ideas and directions for the diagnosis and treatment of HM. In addition, we discuss the role and related mechanisms of HM therapeutic agents targeting the CCL17/CCL22-CCR4 axis and the potential of humanized anti-CCR4 antibodies for the treatment of HM.

摘要

血液系统恶性肿瘤(HM)是发病率和死亡率都很高的常见恶性肿瘤,是严重影响人类健康的恶性疾病,化疗容易复发且有副作用。因此,开发精确、有效且安全的靶向治疗药物已成为当前抗肿瘤技术研究的热点。越来越多的研究表明,C-C趋化因子配体17(CCL17)和C-C趋化因子配体22(CCL22)与受体C-C趋化因子受体4(CCR4)的相互作用促进了肿瘤的免疫逃逸,与血液系统肿瘤的发生、发展及预后密切相关。鉴于此,我们对CCL17/CCL22-CCR4轴在淋巴瘤、白血病和多发性骨髓瘤等血液系统恶性肿瘤中的表达及作用进行综述,旨在为血液系统恶性肿瘤的诊断和治疗提供最新思路和方向。此外,我们还讨论了靶向CCL17/CCL22-CCR4轴的血液系统恶性肿瘤治疗药物的作用及相关机制,以及人源化抗CCR4抗体治疗血液系统恶性肿瘤的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc13/11379839/32fa2f65e54c/12672_2024_1210_Fig1_HTML.jpg

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