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通过人类白细胞抗原介导的免疫逃逸及其对靶向治疗的影响

英文原题:Immune Evasion Through Human Leukocyte Antigen Implications and Its Impact on Targeted Therapy.

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Immune Evasion Through Human Leukocyte Antigen Implications and Its Impact on Targeted Therapy.

PubMed 2024/01/22(内容时间) Cureus

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中文摘要

人类白细胞抗原(HLA)I类抗原的功能异常对白血病治疗效果产生了显著的负面影响,尤其是在依赖T细胞激活的免疫疗法开发中。HLA-G是一种抑制免疫应答的分子,在抑制T细胞、NK 细胞和抗原呈递细胞的激活与增殖中发挥作用。HLA-G的表达与多种病理状态相关。肿瘤细胞利用HLA的免疫逃逸能力,使其能够逃避免疫系统的识别和清除。理解和改造HLA分子对于推进针对慢性淋巴细胞白血病的创新免疫疗法至关重要。为阐明HLA如何在慢性淋巴细胞白血病及其他恶性肿瘤患者中促进肿瘤逃逸,已有大量机制被研究。这些机制包括抑制免疫细胞胞解、改变细胞因子产生水平、促进免疫细胞程序性死亡以及损害趋化作用。本综述全面概述了HLA介导的免疫逃逸及其对靶向治疗的意义。

展开英文摘要原文

The malfunctioning of human leukocyte antigen (HLA) class I antigens has a substantial negative impact on the effectiveness of leukemia treatment, particularly in the development of immunotherapies that rely on T-cell activation. HLA-G, a molecule that suppresses the immune response, plays a role in repressing the activation and proliferation of T cells, natural killer cells, and antigen-presenting cells. The expression of HLA-G is associated with various pathological conditions. Tumor cells exploit the immune evasion capabilities of HLA, allowing them to evade detection and elimination by the immune system.

Understanding and modifying the HLA molecules is crucial for the advancement of innovative immunotherapies targeting chronic lymphocytic leukemia. Numerous mechanisms have been investigated to elucidate how HLA facilitates tumor evasion in patients with chronic lymphocytic leukemia and other malignancies.

These mechanisms include inhibiting immune cell cytolysis, altering cytokine production levels, promoting immune cell programmed cell death, and impairing chemotaxis. This review provides a comprehensive overview of immune evasion mediated by HLA and its implications for targeted therapy.

论文信息

作者
Andreescu M、Andreescu B
第一作者单位
Faculty of Medicine, Titu Maiorescu University, Bucharest, ROU.Romania
通讯作者单位
Plastic Surgery, Colentina Clinical Hospital, Bucharest, ROU.Romania
文献类型
综述
期刊
Cureus2024 Jan
原文标识
PubMed 38384647 · DOI 10.7759/cureus.52737