Cellular immunology最新文献_第6页

Integrated proteomics and phosphoproteomics profiling dynamic signaling networks underlying two distinct types of macrophage activation 综合蛋白质组学和磷酸化蛋白质组学分析两种不同类型巨噬细胞激活的动态信号网络

IF 3.7 4区医学 Q2 CELL BIOLOGY

Cellular immunology

Pub Date : 2025-05-13 DOI: 10.1016/j.cellimm.2025.104972

Lihong Wu , Hang Xu , Xiaonan Zhang , Minghui Zhang , Yuting Xu , Qianyue Zhang , Huiying Tao , Changming Dong , Xinxin Zhang , Mingming Zhou , Jinbo Yang , Chunhua Lin , Qiaoling Song

Macrophages play a crucial role in antimicrobial host defense and those with differential maturation/differentiation status differ in inflammatory responses. Herein, GM-CSF and M-CSF primed mouse bone marrow derived macrophages (GM-BMDMs, GM and M-BMDMs, M), the well-established macrophage models in vitro, were utilized and their dynamic signaling changes in response to gram-negative bacteria component LPS treatment were analyzed using both 4D label-free proteomics and phosphoproteomics. Protein changes maintained relatively constant within or across GM and M macrophages post LPS challenge while phospho-protein exhibited more diverse and transient changes. Early induction of phospho-mediated GTPase activities, mRNA processing, and protein-mediated metabolic changes like oxidative phosphorylation (OXPHOS)/mitochondria function was identified at 1 h and maintained until 6 h post LPS treatment in GM and M while canonical TLR mediated MyD88-dependent and -independent pathways were activated at 3 and 6 h, individually at protein levels. Classical and novel phospho-sites for MyD88 and TRIF signaling pathways were also detected by phosphoproteomics. Comprehensively, the integrated protein and phospho-protein trend analysis was conducted and the core protein-phospho-protein network for the early phase actin reorganization, phagocytosis, and TLR signaling in both GM and M were presented. Taken together, these data described differences and similarities between these two types of macrophages in terms of their inflammatory responses to LPS.

巨噬细胞在抗微生物宿主防御中起着至关重要的作用，具有不同成熟/分化状态的巨噬细胞在炎症反应中存在差异。本研究利用体外建立的巨噬细胞模型GM- csf和M- csf引物小鼠骨髓源性巨噬细胞（GM- bmdms， GM和M- bmdms， M），利用4D无标记蛋白质组学和磷酸化蛋白质组学分析其在革兰氏阴性菌成分LPS处理下的动态信号变化。LPS刺激后，GM和M巨噬细胞内或细胞间的蛋白变化保持相对恒定，而磷酸化蛋白则表现出更多样化和短暂性的变化。早期诱导磷酸化介导的GTPase活性、mRNA加工和蛋白质介导的代谢变化，如氧化磷酸化(OXPHOS)/线粒体功能，在1小时后被鉴定出来，并维持到LPS处理后6小时，而典型的TLR介导的myd88依赖性和非依赖性途径在3和6小时分别在蛋白质水平上被激活。磷酸化蛋白质组学还检测了MyD88和TRIF信号通路的经典和新型磷酸化位点。综合而言，进行了蛋白质和磷酸化蛋白的综合趋势分析，并给出了GM和M早期肌动蛋白重组、吞噬和TLR信号传导的核心蛋白质-磷酸化蛋白网络。综上所述，这些数据描述了这两种巨噬细胞在对LPS的炎症反应方面的异同。

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引用次数: 0

Zinc finger protein 217 contributes to natural killer cell dysfunction in murine colorectal cancer 锌指蛋白217与小鼠结直肠癌自然杀伤细胞功能障碍有关

IF 3.7 4区医学 Q2 CELL BIOLOGY

Cellular immunology

Pub Date : 2025-05-10 DOI: 10.1016/j.cellimm.2025.104971

Yibing Yu , Huanbin Yang , Hao Wang , Fei Xiao

Immune cells play active roles in the surveillance and control of colorectal cancer (CRC) progression. Natural killer (NK) cells are powerful anti-tumor effector cells but their regulatory mechanisms in the CRC tissues have not been thoroughly elucidated. In this research using a murine inflammatory colorectal cancer model, we characterized the phenotype and function of NK cells. We found signs of NK cell dysfunction in CRC tissues, including up-regulation of exhaustion markers, down-regulation of activating receptors, deficiencies in degranulation and cytokine expression, and weak cytolytic effect. Interestingly, zinc finger protein 217 (ZNF217), a transcription repressor, was significantly up-regulated in CRC-associated NK cells. In vitro assays revealed that ZNF217 knockdown promoted NK cell cytolytic activity, implying that ZNF217 is an inhibitory factor of NK cell function. Adoptive transfer assays indicated that ZNF217 knockdown also resulted in enhancement of NK cell function in vivo and subsequently suppressed CRC development. Furthermore, hypoxia rather than exhaustion up-regulated ZNF217 expression in NK cells. ZNF217 knockdown promoted NK cell resistance to hypoxia-mediated NK cell dysfunction. Therefore, we discovered a novel regulatory factor of NK cell dysfunction during CRC development.

免疫细胞在监测和控制结直肠癌（CRC）进展中发挥积极作用。自然杀伤细胞（NK）是一种强大的抗肿瘤效应细胞，但其在结直肠癌组织中的调控机制尚未完全阐明。在本研究中，我们利用小鼠炎性结直肠癌模型，表征NK细胞的表型和功能。我们在结直肠癌组织中发现NK细胞功能障碍的迹象，包括衰竭标志物上调，激活受体下调，脱颗粒和细胞因子表达不足，细胞溶解作用弱。有趣的是，锌指蛋白217 (ZNF217)，一种转录抑制因子，在crc相关的NK细胞中显著上调。体外实验显示，ZNF217敲低可促进NK细胞的细胞溶解活性，提示ZNF217是NK细胞功能的抑制因子。过继转移实验表明，ZNF217敲低也导致体内NK细胞功能增强，随后抑制结直肠癌的发展。此外，缺氧而非衰竭上调了NK细胞中ZNF217的表达。ZNF217敲低可促进NK细胞对缺氧介导的NK细胞功能障碍的抵抗。因此，我们发现了在结直肠癌发展过程中NK细胞功能障碍的一个新的调节因子。

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引用次数: 0

Investigating the effect of neuro-immune communication on immune responses in health and disease: Exploring immunological disorders 研究健康和疾病中神经免疫通讯对免疫反应的影响：探索免疫紊乱

IF 3.7 4区医学 Q2 CELL BIOLOGY

Cellular immunology

Pub Date : 2025-05-09 DOI: 10.1016/j.cellimm.2025.104963

Fatemeh Hesampour , Charles N. Bernstein , Jean-Eric Ghia

Recent recognition of the intricate nervous-immune system interplay has prompted research into the specific cellular components involved in these interactions. Emerging evidence suggests that immune and neural cells collaborate within distinct units and act in concert to regulate tissue function and provide protection. These specialized neuro-immune cell units have been identified in diverse body tissues, ranging from lymphoid organs to the bone marrow and mucosal barriers. Their significance has become increasingly apparent as they are recognized as pivotal regulators influencing a broad spectrum of physiological and pathological processes. This recognition extends to critical roles in hematopoiesis, organ function, inflammatory responses, and intricate tissue repair processes. This review explores the bidirectional communication between the nervous and immune systems. The focus is on understanding the profound impact of this communication on immune cells within key anatomical sites, such as the bone marrow, gastrointestinal tract, and lymphoid organs. By examining these interactions, this review aims to shed light on how this intricate network operates under normal and pathological conditions, offering insights into the mechanisms underlying health and disease.

最近对复杂的神经-免疫系统相互作用的认识促使人们对参与这些相互作用的特定细胞成分进行了研究。新出现的证据表明，免疫细胞和神经细胞在不同的单位内协作，共同调节组织功能并提供保护。这些特殊的神经免疫细胞单位已经在不同的身体组织中被发现，从淋巴器官到骨髓和粘膜屏障。它们的重要性已经变得越来越明显，因为它们被认为是影响广泛的生理和病理过程的关键调节因子。这种认识延伸到造血、器官功能、炎症反应和复杂的组织修复过程的关键作用。本文综述了神经系统和免疫系统之间的双向交流。重点是了解这种交流对关键解剖部位（如骨髓、胃肠道和淋巴器官）免疫细胞的深远影响。通过研究这些相互作用，本综述旨在揭示这个复杂的网络在正常和病理条件下是如何运作的，为健康和疾病的潜在机制提供见解。

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引用次数: 0

Progress of exosomes in regulating tumor metastasis by remodeling the pre-metastatic immune microenvironment 外泌体通过重塑转移前免疫微环境调控肿瘤转移的研究进展

IF 3.7 4区医学 Q2 CELL BIOLOGY

Cellular immunology

Pub Date : 2025-05-09 DOI: 10.1016/j.cellimm.2025.104960

Jiangning Xiang, Lin Yao, Shan Wang, Lei Zhao, Jing Yu

Exosomes play an important role in the metastatic microenvironment, acting as a transmission belt that facilitates intercellular communication. By delivering proteins, nucleic acids, and other substances in the exosomes, they can change the function of the receptor target cells, change the microenvironment of the metastatic site, and promote the colonization of the tumor cells, thus promoting cancer metastasis. The interaction between tumor cells and the surrounding microenvironment is complex, with exosomes serving as key facilitators of crosstalk between the primary tumor microenvironment and the pre-metastasis microenvironment. Despite many current studies to explore exosomes, we still do not have a detailed understanding of the role and mechanism of exosomes in the pre-metastatic immune microenvironment, and there are many challenges in the clinical application of exosomes. In this paper, we summarize the role of exosomes in regulating the pre-metastatic immune microenvironment and its mechanism, focusing on how exosomes regulate the function of immune cells in the pre-metastatic microenvironment to promote tumor metastasis. In addition, the potential application of exosomes in tumor immunotherapy and strategies for targeting exosomes are discussed. This will contribute to the immunotherapy of cancer metastasis and promote the clinical application of exosomes.

外泌体在转移性微环境中发挥重要作用，作为促进细胞间通讯的传输带。它们通过在外泌体中传递蛋白质、核酸等物质，改变受体靶细胞的功能，改变转移部位的微环境，促进肿瘤细胞的定植，从而促进癌症转移。肿瘤细胞与周围微环境之间的相互作用是复杂的，外泌体是原发肿瘤微环境与转移前微环境之间串扰的关键促进因子。尽管目前有许多研究对外泌体进行了探索，但我们对外泌体在转移前免疫微环境中的作用和机制仍然没有详细的了解，外泌体的临床应用存在许多挑战。本文综述了外泌体调控肿瘤转移前免疫微环境的作用及其机制，重点阐述了外泌体调控肿瘤转移前免疫微环境中免疫细胞的功能，促进肿瘤转移的机制。此外，还讨论了外泌体在肿瘤免疫治疗中的潜在应用以及靶向外泌体的策略。这将有助于肿瘤转移的免疫治疗，促进外泌体的临床应用。

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引用次数: 0

Modular activation of macrophage-like cells by beta-2-microglobulin via mitochondria and the cGAS-STING pathway β -2微球蛋白通过线粒体和cGAS-STING途径模块化激活巨噬细胞样细胞

IF 3.7 4区医学 Q2 CELL BIOLOGY

Cellular immunology

Pub Date : 2025-05-05 DOI: 10.1016/j.cellimm.2025.104962

Josefine Kofoed Corneliussen , Helena Borland Madsen , Nadia Thaulov Zelander , Mogens Holst Nissen , Claus Desler

Beta-2-microglobulin (β2m) is a component of the major histocompatibility complex class I. β2m is released into cellular fluids in response to various stimuli, including pro-inflammatory cytokines. Elevated β2m levels have been found associated with autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, and Crohn's disease, as well as in various hematological cancers and viral infections. Despite an established correlation between immune activation of especially monocytes and macrophages, and circulating β2m levels, the causative relationship remains unclear. Here, we investigate the effects of exogenous β2m and a complement C1s cleaved form, dK58β2m, on two murine macrophage-like cell lines J774 and RAW. We demonstrate that β2m, and to a greater extent dK58β2m, can affect mitochondrial activity. Furthermore, the presence of IFN-γ amplifies the effect, causing altered bioenergetics, and increased production of mitochondrial reactive oxygen species and nitric oxide. In addition, we found activation of the cGAS-STING pathway by β2m and dK58β2m in the presence of IFN-γ. Only dK58β2m in combination with IFN-γ caused apoptosis and cell death. Our findings highlight the modular nature of a β2m-induced macrophage response, potentiated by dK58β2m and IFN-γ, and provide information on the underlying mechanisms responsible for the immune activation properties of β2m.

β -2微球蛋白（β2m）是主要组织相容性复合体i类的一个组成部分。β2m在各种刺激下释放到细胞液中，包括促炎细胞因子。已发现β2m水平升高与自身免疫性疾病，如类风湿关节炎、系统性红斑狼疮和克罗恩病，以及各种血液学癌症和病毒感染有关。尽管免疫激活（尤其是单核细胞和巨噬细胞）与循环β2m水平之间存在明确的相关性，但致病关系尚不清楚。在这里，我们研究了外源性β2m和补体C1s切割形式dK58β2m对两种小鼠巨噬细胞样细胞系J774和RAW的影响。我们证明β2m，以及在更大程度上dK58β2m可以影响线粒体活性。此外，IFN-γ的存在放大了这种效应，导致生物能量学的改变，并增加了线粒体活性氧和一氧化氮的产生。此外，我们发现在IFN-γ存在下，β2m和dK58β2m激活了cGAS-STING通路。仅dK58β2m与IFN-γ联合引起细胞凋亡和死亡。我们的研究结果强调了β2m诱导的巨噬细胞反应的模块化性质，由dK58β2m和IFN-γ增强，并提供了有关β2m免疫激活特性的潜在机制的信息。

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引用次数: 0

miRNA-186-5p modulates placental inflammation via Inflammasome activation in gestational diabetes mellitus miRNA-186-5p通过炎症小体激活调节妊娠糖尿病胎盘炎症

IF 3.7 4区医学 Q2 CELL BIOLOGY

Cellular immunology

Pub Date : 2025-05-01 DOI: 10.1016/j.cellimm.2025.104959

Bhatnagar Megha , K.L. Milan , M. Anuradha , Kunka Mohanram Ramkumar

Inflammasomes are multiprotein complexes that initiate inflammatory responses by activating pro-inflammatory cytokines, playing a crucial role in innate immunity. However, their dysregulation can lead to excessive inflammation, particularly in conditions like gestational diabetes mellitus (GDM), where placental inflammation may adversely affect fetal development and increase the risk of complications. NEK7 (NIMA-related kinase 7) has been identified as a key mediator in inflammasome activation, facilitating the complex assembly and amplifying inflammatory responses. This study aims to investigate the regulatory role of miRNA in inflammasome-mediated placental inflammation through its interaction with NEK7 in the pathophysiology of GDM. In-silico analysis identified that NEK7 is a direct target of miR-186-5p, while PCR analysis demonstrated a significant loss of miR-186-5p expression in GDM placental tissues. Further, the expressions of NEK7, NLRP1, NLRP3, Caspase 1 along with the inflammatory cytokines were significantly elevated in GDM placenta. Furthermore, the correlation analysis demonstrated a significant negative correlation between miR-186-5p and NEK7 expression levels, suggesting that the loss of miR-186-5p may contribute to inflammasome mediated placental inflammation in GDM. Additionally, the overexpression of miR-186-5p decreased the high glucose induced inflammation and the expressions of NEK7, NLRP1 and NLRP3 in BeWo cell line. Therefore, this study concludes that miR-186-5p may attenuate the activation of inflammasome and regulate inflammation via NEK7 in the progression of GDM. Understanding these molecular mechanisms offers valuable insights into potential therapeutic targets aimed at improving pregnancy outcomes in GDM.

炎性小体是一种多蛋白复合物，通过激活促炎细胞因子引发炎症反应，在先天免疫中起着至关重要的作用。然而，它们的失调会导致过度炎症，特别是在妊娠糖尿病（GDM）等情况下，胎盘炎症可能会对胎儿发育产生不利影响，并增加并发症的风险。NEK7 （nima相关激酶7）已被确定为炎症小体激活的关键介质，促进复合物组装和放大炎症反应。本研究旨在通过miRNA与NEK7在GDM病理生理中的相互作用，探讨miRNA在炎症小体介导的胎盘炎症中的调节作用。计算机分析发现NEK7是miR-186-5p的直接靶点，而PCR分析显示GDM胎盘组织中miR-186-5p的表达明显缺失。此外，GDM胎盘中NEK7、NLRP1、NLRP3、Caspase 1及炎性因子的表达均显著升高。此外，相关分析显示miR-186-5p与NEK7表达水平呈显著负相关，表明miR-186-5p的缺失可能导致GDM中炎症小体介导的胎盘炎症。此外，过表达miR-186-5p可降低BeWo细胞系高糖诱导的炎症以及NEK7、NLRP1和NLRP3的表达。因此，本研究认为miR-186-5p可能在GDM的进展中减弱炎性小体的激活，并通过NEK7调节炎症。了解这些分子机制为改善GDM妊娠结局的潜在治疗靶点提供了有价值的见解。

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引用次数: 0

Potential therapeutic strategies targeting efferocytosis for inflammation resolution and tissue repair in inflammatory bowel disease 在炎症性肠病中针对efferocytosis的炎症消退和组织修复的潜在治疗策略

IF 3.7 4区医学 Q2 CELL BIOLOGY

Cellular immunology

Pub Date : 2025-05-01 DOI: 10.1016/j.cellimm.2025.104957

Chaoquan Li , Wanting Liu , Aoni Fu , Haotian Yang , Guanghui Yi

Efferocytosis, the process by which apoptotic cells (ACs) are recognized and cleared by phagocytes, is a critical mechanism in maintaining intestinal immune homeostasis and promoting the resolution of inflammation. Inflammatory bowel disease (IBD), encompassing Crohn's disease (CD) and ulcerative colitis (UC), is characterized by chronic intestinal inflammation, wherein defective efferocytosis contributes to the accumulation of ACs, secondary necrosis, and sustained mucosal damage. This review delineates the molecular mechanisms underlying efferocytosis and systematically examines its functional roles across five key intestinal phagocytic cell types: macrophages, dendritic cells (DCs), neutrophils, intestinal epithelial cells (IECs), and Paneth cells (PCs). Particular emphasis is placed on the dysregulation of efferocytosis capacity in IBD pathogenesis and the consequences of impaired apoptotic cell clearance in both professional and non-professional phagocytes. Furthermore, we evaluate emerging therapeutic strategies designed to restore or enhance efferocytosis, including modulation of macrophage polarization, LC3-associated phagocytosis pathways, nanotechnology-enabled delivery systems, and stem cell-based interventions. A comprehensive understanding of cell-type-specific efferocytosis in the intestinal microenvironment offers promising directions for the development of targeted, inflammation-resolving therapies for IBD.

Efferocytosis是凋亡细胞被吞噬细胞识别和清除的过程，是维持肠道免疫稳态和促进炎症消退的关键机制。炎症性肠病（IBD），包括克罗恩病（CD）和溃疡性结肠炎（UC），其特征是慢性肠道炎症，其中有缺陷的efferocytosis有助于ACs的积累，继发性坏死和持续的粘膜损伤。本文综述了efferocytosis的分子机制，并系统地研究了其在五种主要肠道吞噬细胞类型中的功能作用：巨噬细胞、树突状细胞（dc）、中性粒细胞、肠上皮细胞（IECs）和Paneth细胞（PCs）。特别强调的是在IBD发病机制中efferocytocapacity的失调以及在专业和非专业吞噬细胞中受损的凋亡细胞清除的后果。此外，我们评估了旨在恢复或增强efferocytosis的新兴治疗策略，包括巨噬细胞极化的调节、lc3相关的吞噬途径、纳米技术支持的递送系统和基于干细胞的干预。全面了解肠道微环境中细胞类型特异性的efferocytosis，为开发针对IBD的炎症解决疗法提供了有希望的方向。

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引用次数: 0

Immunity in children: How does it begin? 儿童免疫：它是如何开始的？

IF 3.7 4区医学 Q2 CELL BIOLOGY

Cellular immunology

Pub Date : 2025-05-01 DOI: 10.1016/j.cellimm.2025.104945

Simon Fillatreau

引用次数: 0

The NLRP3 Inflammasome in inflammatory diseases: Cellular dynamics and role in granuloma formation 炎性疾病中的NLRP3炎性小体：细胞动力学及其在肉芽肿形成中的作用

IF 3.7 4区医学 Q2 CELL BIOLOGY

Cellular immunology

Pub Date : 2025-05-01 DOI: 10.1016/j.cellimm.2025.104961

Isadora M. de Oliveira , Mariana M. Chaves

The innate immune system recognizes pathogen-associated molecular patterns (PAMPs) and damage associated molecular patterns (DAMPs) through pattern recognition receptors (PRRs). Inflammasomes, cytoplasmic protein complexes, are activated in response to PAMPs and DAMPs, leading to the release of inflammatory cytokines such as IL-1β and IL-18. NLRP3 inflammasome is one of the best characterized inflammasomes and recently its activation has been associated with granuloma formation, structures that aggregate immune cells in response to infections, such as those caused by bacteria, fungi and parasites, and autoinflammatory diseases, such as sarcoidosis. Activation of NLRP3 inflammasomes in macrophages induces the release of cytokines that recruit immune cells, such as monocytes and lymphocytes, to the site of infection. Neutrophils, monocytes, T and B lymphocytes are important in the formation and maintenance of granulomas. Although NLRP3 plays a key role in the immune response, cell recruitment and granuloma formation, many aspects of its function in different cell types remain to be elucidated. In this review, we aim to outline the NLRP3 inflammasome not only as a protein complex that aids innate immune cells in combating intracellular pathogens but also as a platform with broader implications in orchestrating immune responses. This underexplored aspect of the NLRP3 inflammasome presents a novel perspective on its involvement in immunity. Thus, we review the current understanding of the role of the NLRP3 inflammasome in immune cell infiltration and its significance in the organization and formation of granulomas in inflammatory diseases.

先天免疫系统通过模式识别受体（PRRs）识别病原体相关分子模式（PAMPs）和损伤相关分子模式（DAMPs）。炎性小体，细胞质蛋白复合物，在PAMPs和DAMPs的响应下被激活，导致炎症细胞因子如IL-1β和IL-18的释放。NLRP3炎性小体是最具特征的炎性小体之一，最近它的激活与肉芽肿的形成有关，肉芽肿是免疫细胞聚集以应对感染的结构，如由细菌、真菌和寄生虫引起的感染，以及自身炎症性疾病，如结节病。巨噬细胞中NLRP3炎性小体的激活诱导细胞因子的释放，这些细胞因子将免疫细胞（如单核细胞和淋巴细胞）招募到感染部位。中性粒细胞、单核细胞、T淋巴细胞和B淋巴细胞在肉芽肿的形成和维持中起重要作用。尽管NLRP3在免疫应答、细胞募集和肉芽肿形成中起着关键作用，但其在不同细胞类型中的许多功能仍有待阐明。在这篇综述中，我们的目标是概述NLRP3炎性小体不仅是一种蛋白质复合物，帮助先天免疫细胞对抗细胞内病原体，而且在协调免疫反应方面具有更广泛的意义。NLRP3炎症小体的这一未被充分探索的方面为其参与免疫提供了一个新的视角。因此，我们对NLRP3炎性小体在免疫细胞浸润中的作用及其在炎症性疾病肉芽肿组织形成中的意义进行综述。

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引用次数: 0

The real-world impact of corticosteroid-associated adverse events in myasthenia gravis: A patient-reported survey analysis 在重症肌无力中，皮质类固醇相关不良事件的实际影响：一项患者报告的调查分析

IF 3.7 4区医学 Q2 CELL BIOLOGY

Cellular immunology

Pub Date : 2025-05-01 DOI: 10.1016/j.cellimm.2025.104956

Jinyi Yan , Kalam Choi , Peicai Fu, Mengge Yang, Jing Lin, Mengcui Gui, Yue Li, Bitao Bu, Zhijun Li

Background

Corticosteroids are crucial for managing acute exacerbation symptoms and preventing relapses in myasthenia gravis (MG) patients.

Methods

Between April 15–30, 2024, 2368 online self - report questionnaires were distributed. Eventually, 444 MG patients who had received corticosteroid therapy completed the survey.

Results

Self-reported adverse events (AEs) were observed in 97.5 % of the respondents. Among them, 72.5 % (322 patients) reported experiencing more than four AEs. The quality of life (QOL) of patients with MG was significantly impacted, with average MG-QOL scores of 18.07 ± 12.03. Patients with a cumulative dosage exceeding 20 g experienced the highest incidence of various AEs compared to those with lower cumulative dosages (5–20 g and less than 5 g). Additionally, a longer duration of corticosteroid exposure was associated with a higher reported incidence of AEs. Cox risk regression modeling revealed that a longer disease course, a history of myasthenic crisis, and the average daily dose of steroids (exceeding 5 mg/d), were independent predictors of corticosteroid-associated AEs. The study revealed in a single MG center, the awareness of these AEs was low among Chinese patients.

Conclusion

This study systematically assessed the incidence and risk factors of corticosteroid-related AEs in Chinese MG patients. The study found that the occurrence of AEs was associated with the cumulative dosage and duration of corticosteroid use. Additionally, long disease duration, a history of myasthenic crises, and an average daily dosage exceeding 5 mg/d are identified as risk factors for corticosteroid-related AEs in patients with MG.

背景：皮质类固醇对于控制重症肌无力（MG）患者的急性加重症状和预防复发至关重要。方法于2024年4月15日至30日，发放网上自述问卷2368份。最终，444名接受皮质类固醇治疗的MG患者完成了调查。结果97.5%的应答者有自我报告不良事件（ae）。其中，72.5%（322例）报告经历了4次以上ae。MG患者的生活质量（QOL）明显受到影响，MG-QOL平均评分为18.07±12.03分。累积剂量超过20g的患者与较低累积剂量（5 - 20g和小于5g）的患者相比，各种不良反应的发生率最高。此外，较长的皮质类固醇暴露时间与较高的不良反应发生率相关。Cox风险回归模型显示，病程较长、有肌无力危象史和平均每日类固醇剂量（超过5mg /d）是皮质类固醇相关不良事件的独立预测因素。该研究显示，在一个MG中心，中国患者对这些不良事件的认识较低。结论本研究系统评估了中国MG患者皮质类固醇相关不良事件的发生率及危险因素。研究发现，不良事件的发生与皮质类固醇使用的累积剂量和持续时间有关。此外，病程长、肌无力危象史和平均每日剂量超过5mg /d被确定为mg患者皮质类固醇相关ae的危险因素。

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引用次数: 0