Current Opinion in Immunology最新文献

英文中文

Challenges in diagnosis of sarcoidosis 结节病诊断的挑战

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-12-01 Epub Date: 2025-09-01 DOI: 10.1016/j.coi.2025.102652

Karol Bączek , Wojciech J Piotrowski , Francesco Bonella

Purpose of review

Diagnosing sarcoidosis remains challenging. Histology findings and a variable clinical presentation can mimic other infectious, malignant, and autoimmune diseases. This review synthesizes current evidence on histopathology, sampling techniques, imaging modalities, and biomarkers and explores how emerging ‘omics’ and artificial intelligence tools may sharpen diagnostic accuracy.

Recent findings

Within the typical granulomatous lesions, limited or ‘burned-out’ necrosis is an ancillary finding, which can be present in up to one-third of sarcoid biopsies, and demands a careful differential diagnostic work-up. Endobronchial ultrasound–guided transbronchial needle aspiration of lymph nodes has replaced mediastinoscopy as first-line sampling tool, while cryobiopsy is still under validation. Volumetric PET metrics such as total lung glycolysis and somatostatin-receptor tracers refine activity assessment; combined FDG PET/MRI improves detection of occult cardiac disease. Advanced bronchoalveolar lavage (BAL) immunophenotyping via flow cytometry and serum, BAL, and genetic biomarkers show to correlate with inflammatory burden but have low diagnostic value. Multi-omics signatures and Positron Emission Tomography with Computer Tomography radiomics, supported by deep-learning algorithms, show promising results for noninvasive diagnostic confirmation, phenotyping, and disease monitoring.

Summary

No single test is conclusive for diagnosing sarcoidosis. An integrated, multidisciplinary strategy is needed. Large, multicenter, and multiethnic studies are essential to translate and validate data from emerging AI tools and -omics research into clinical routine.

综述的目的结节病的诊断仍然具有挑战性。组织学表现和可变的临床表现可以模仿其他感染性、恶性和自身免疫性疾病。本综述综合了组织病理学、采样技术、成像模式和生物标志物方面的现有证据，并探讨了新兴的“组学”和人工智能工具如何提高诊断准确性。最近的发现在典型的肉芽肿病变中，局限性或“烧坏性”坏死是一种辅助发现，可出现在高达三分之一的肉瘤活检中，需要仔细的鉴别诊断检查。支气管超声引导下经支气管淋巴结穿刺已经取代纵隔镜作为一线取样工具，低温活检仍处于验证阶段。容积PET指标，如肺总糖酵解和生长抑素受体示踪剂，改进了活性评估；FDG PET/MRI联合检测可提高隐匿性心脏病的检出率。晚期支气管肺泡灌洗（BAL）免疫表型通过流式细胞术和血清，BAL和遗传生物标志物显示与炎症负担相关，但诊断价值低。在深度学习算法的支持下，多组学签名和正电子发射断层扫描与计算机断层放射组学在无创诊断确认、表型和疾病监测方面显示出有希望的结果。没有单一的检查对结节病的诊断具有结论性。需要一个综合的多学科战略。大型、多中心、多民族的研究对于将新兴人工智能工具和组学研究的数据转化和验证为临床常规至关重要。

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引用次数: 0

Approved and emerging therapies for glucocorticoid-refractory chronic graft-versus-host disease 经批准和新兴的治疗糖皮质激素难治性慢性移植物抗宿主病的方法

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-12-01 Epub Date: 2025-09-09 DOI: 10.1016/j.coi.2025.102654

Xinwen Zhang , Yuxin Ren , Ruihao Huang , Xiaoqi Wang , Xi Zhang

Glucocorticoid-refractory chronic graft-versus-host disease (glucocorticoid-refractory cGVHD) remains a major barrier to long-term survival and quality of life following allogeneic hematopoietic stem cell transplantation (allo-HSCT), affecting 30–70% to half of patients with chronic GVHD who fail corticosteroid therapy. In recent years, the Food and Drug Administration (FDA) has approved four agents — ibrutinib, ruxolitinib, belumosudil, and axatilimab — each targeting distinct immune and fibrotic pathways. This review systematically evaluates their mechanisms of action, efficacy across organ systems, and safety profiles while highlighting persistent limitations. We further summarize emerging therapies in clinical and preclinical development, including kinase inhibitors, monoclonal antibodies, cellular approaches, and tissue-specific interventions. A dual-axis framework — distinguishing inflammatory versus fibrotic phenotypes and organ-specific manifestations — is proposed to support biomarker-guided, individualized treatment. In addition, combination regimens and AI-assisted strategies offer new opportunities to optimize outcomes and reduce treatment burden. Despite these advances, challenges remain, including irreversible fibrosis, disease heterogeneity, lack of standardized diagnostic criteria, and balanced GVHD and graft versus tumor effect. Greater incorporation of patient-reported outcomes and long-term functional assessments into clinical trials and practice is urgently needed. Collectively, this review offers a roadmap for optimizing glucocorticoid-refractory cGVHD management, and evolving strategies hold promise for transforming glucocorticoid-refractory cGVHD from a life-limiting condition into a manageable chronic disease.

糖皮质激素难治性慢性移植物抗宿主病（糖皮质激素难治性cGVHD）仍然是同种异体造血干细胞移植（alloo - hsct）后长期生存和生活质量的主要障碍，影响了30-70%至一半皮质类固醇治疗失败的慢性GVHD患者。近年来，美国食品和药物管理局（FDA）批准了四种药物——依鲁替尼、鲁索利替尼、白莫沙地尔和阿替利单抗——每一种都针对不同的免疫和纤维化途径。这篇综述系统地评估了它们的作用机制、跨器官系统的有效性和安全性，同时强调了持续的局限性。我们进一步总结了临床和临床前开发的新兴疗法，包括激酶抑制剂、单克隆抗体、细胞方法和组织特异性干预。双轴框架-区分炎症与纤维化表型和器官特异性表现-被提出支持生物标志物引导的个体化治疗。此外，联合方案和人工智能辅助策略为优化结果和减轻治疗负担提供了新的机会。尽管取得了这些进展，但挑战仍然存在，包括不可逆纤维化、疾病异质性、缺乏标准化的诊断标准、GVHD和移植物与肿瘤效应的平衡。迫切需要在临床试验和实践中更多地纳入患者报告的结果和长期功能评估。总之，这篇综述为优化糖皮质激素难治性cGVHD的管理提供了一个路线图，并且不断发展的策略有望将糖皮质激素难治性cGVHD从限制生命的疾病转变为可控制的慢性疾病。

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引用次数: 0

From genes to granulomas: the genetic blueprint of sarcoidosis 从基因到肉芽肿：结节病的基因蓝图。

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-12-01 Epub Date: 2025-09-19 DOI: 10.1016/j.coi.2025.102663

Martin Petrek , Natalia V Rivera

Sarcoidosis is a complex, polygenic, and multifactorial disease characterized by granulomas in affected organs, which are the hallmark of the condition. Genetic susceptibility, environmental influences, and lifestyle factors play key roles in its development. Although the exact molecular mechanisms are not yet fully understood, it is known that the immune system plays a role in mediating the disease. Additionally, sarcoidosis encompasses a group of disease entities (endophenotypes) whose clinical features and progression can be described to help improve understanding of their genetic architecture. In this work, we aim to review recent advances in the genetics and immunopathogenesis of sarcoidosis and explore future directions to improve clinical outcomes and achieve the goals of precision medicine.

结节病是一种复杂的、多基因的、多因素的疾病，其特征是受累器官中的肉芽肿，这是该病的标志。遗传易感性、环境影响和生活方式因素在其发展中起关键作用。虽然确切的分子机制尚不完全清楚，但已知免疫系统在介导疾病中起作用。此外，结节病包括一组疾病实体（内表型），其临床特征和进展可以被描述，以帮助提高对其遗传结构的理解。本文就结节病的遗传学和免疫发病机制的最新进展进行综述，探讨未来的研究方向，以提高结节病的临床疗效，实现精准医疗的目标。

引用次数: 0

COVID-19 and inflammatory bowel disease — what to know COVID-19和炎症性肠病——需要了解什么？

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-12-01 Epub Date: 2025-09-30 DOI: 10.1016/j.coi.2025.102661

Anne Godat , Dimitrios Chistoforidis , Thomas Greuter

Inflammatory bowel disease (IBD) represents a chronic inflammation of the gastrointestinal tract that arises from a complex interplay between a dysregulated immune response in genetically predisposed individuals. IBD can further be classified into its two main subtypes, Crohn’s disease and ulcerative colitis. Both subtypes have shown increasing prevalence and incidence rates worldwide, and IBD is now considered a global epidemic. About three million patients are estimated to suffer from this disease, both in the US and Europe, with most of them requiring maintenance treatment including immunosuppressive agents, putting them at risk for opportunistic infections. In 2020, coronavirus disease 2019 (COVID-19) hit the world with a long pandemic period resulting in dramatic numbers of hospitalizations, Intensive care unit (ICU) admissions, and deaths. Patients with chronic illnesses, such as IBD, were rapidly considered to be at an increased risk for both infection and infection-related complications. For IBD and its treatment, however, evidence over the last few years showed no increased risk for SARS-CoV-2 infection or COVID-related complications. In this review, we will discuss the latest insights about COVID-19 in IBD patients with a particular focus on the disease course of COVID-19 and on IBD-related adverse outcomes.

炎症性肠病（IBD）是一种胃肠道慢性炎症，由遗传易感个体的免疫反应失调之间的复杂相互作用引起。IBD可以进一步分为两个主要亚型，克罗恩病和溃疡性结肠炎。这两种亚型在世界范围内的流行率和发病率都在增加，IBD现在被认为是一种全球流行病。在美国和欧洲，估计约有300万患者患有这种疾病，其中大多数人需要维持治疗，包括免疫抑制剂，这使他们面临机会性感染的风险。2020年，2019年冠状病毒病（COVID-19）在全球流行了很长时间，导致大量住院、重症监护病房（ICU）入院和死亡。患有慢性疾病（如IBD）的患者很快被认为感染和感染相关并发症的风险增加。然而，对于IBD及其治疗，过去几年的证据显示，SARS-CoV-2感染或covid相关并发症的风险没有增加。在这篇综述中，我们将讨论关于COVID-19在IBD患者中的最新见解，特别关注COVID-19的病程和IBD相关的不良结局。

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引用次数: 0

Deciphering and harnessing gut microbiota–associated immune regulation in acute graft-versus-host disease 在急性移植物抗宿主病中破译和利用肠道微生物群相关的免疫调节

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-12-01 Epub Date: 2025-10-10 DOI: 10.1016/j.coi.2025.102676

Emmanuelle Godefroy , Frédéric Altare

Allogeneic hematopoietic stem cell transplantation represents a curative treatment of choice for numerous severe hematological malignancies. While donor-derived transplanted T cells can limit disease relapse (GvT/GvL effect), they also induce, in 30–50% of the patients, acute graft-versus-host disease (aGvHD), a severe condition with elevated mortality and comorbidity rates. Gut microbiota composition has been associated with aGvHD outcome. This observation created a substantial research interest, and individual gut microbiota commensals have been acknowledged for their ability to promote immune regulation, both locally and systemically, and thus limit aGvHD-related inflammation. The mechanisms by which commensals support immune homeostasis are being decrypted at a remarkable rate. However, the trillions of micro-organisms comprising the gut microbiome interact, both directly and indirectly, with local immune cells, which is all the more critical in the context of heavy conditioning regimens these patients undergo, themselves damaging mucosal tissues and prompting inflammation. Commensals can help preserve the gut barrier integrity by actively limiting deleterious inflammation processes. Mechanistically deciphering the intricate crosstalk between gut microbes and gut immune cells, both at the species level and globally, represents a colossal challenge, but holds great promise in predicting and harnessing numerous pathological processes, including aGvHD. This review aims to examine the acquired knowledge concerning immunoregulatory responses driven by gut microbiota in the context of aGvHD. Recent preclinical and clinical studies harnessing such pathways proved to be encouraging, while substantial hurdles subsist regarding how to successfully harness this complex host/microbiota interplay to constrain aGvHD.

同种异体造血干细胞移植是治疗许多严重血液系统恶性肿瘤的一种选择。虽然供体来源的移植T细胞可以限制疾病复发（GvT/GvL效应），但它们也会在30-50%的患者中诱发急性移植物抗宿主病（aGvHD），这是一种死亡率和合并症发生率升高的严重疾病。肠道菌群组成与aGvHD的预后有关。这一观察结果引起了大量的研究兴趣，并且个体肠道微生物群共生体因其促进局部和全身免疫调节的能力而得到承认，从而限制了agvhd相关的炎症。共生体支持免疫稳态的机制正在以惊人的速度被解密。然而，组成肠道微生物组的数万亿微生物直接或间接地与局部免疫细胞相互作用，这在这些患者接受大量调理方案的背景下更为关键，它们本身会损害粘膜组织并引发炎症。共生菌可以通过积极地限制有害的炎症过程来帮助保持肠道屏障的完整性。在物种水平和全球范围内，从机制上破译肠道微生物和肠道免疫细胞之间复杂的串扰是一个巨大的挑战，但在预测和利用包括aGvHD在内的许多病理过程方面具有很大的希望。本综述旨在研究在aGvHD背景下肠道微生物群驱动的免疫调节反应的相关知识。最近利用这些途径的临床前和临床研究被证明是令人鼓舞的，然而在如何成功利用这种复杂的宿主/微生物群相互作用来限制aGvHD方面存在实质性障碍。

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引用次数: 0

Microglia and myeloperoxidase in neuroinflammatory and neurodegenerative diseases 神经炎症和神经退行性疾病中的小胶质细胞和髓过氧化物酶。

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-12-01 Epub Date: 2025-09-18 DOI: 10.1016/j.coi.2025.102660

Lorenzo Del Moro , Enrico Brunetta , M. Eric Gershwin , Carlo Selmi

The dogma of an impenetrable blood–brain barrier (BBB) has given way to the view that resident immune cells within the central nervous system respond to a variety of blood-borne soluble factors, particularly cytokines, and play an important functional role. In particular, microglia cells contribute to the regulation of neuroinflammation, with both protective and pathological roles. Specific microglia activation states variably influence the progression of neuroinflammatory and neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, multiple sclerosis, and amyotrophic lateral sclerosis. Significant evidence indicates that gut microbiota–derived products regulate microglial function across the lifespan and influence the BBB. Myeloperoxidase (MPO) catalyzes the conversion of hydrogen peroxide and chloride ions into hypochlorous acid, a potent oxidant implicated in oxidative tissue damage and modulation of inflammatory signaling. Elevated MPO levels in the central nervous system have been correlated with human disease and the dysregulation of MPO activity in microglia is particularly detrimental, as it amplifies the oxidative stress, disrupts the BBB integrity, and potentiates the neuroinflammatory cascades through the activation of transcription factors like NF-κB. Targeting MPO activity through selective inhibitors or antioxidant strategies may attenuate microglial activation and reduce neuroinflammation, highlighting its potential as a therapeutic target, but the regulatory mechanisms governing MPO expression in microglia and its interplay with other inflammatory mediators remain poorly understood. New research efforts into the relationship between gut microbiota, microglia, MPO, and neuroinflammation are essential to unravel the complexities of neuropathology in a variety of conditions beyond neurodegenerative diseases.

不可逾越的血脑屏障（BBB）的教条已经让位于中枢神经系统内驻留的免疫细胞对各种血源性可溶性因子，特别是细胞因子作出反应，并发挥重要的功能作用的观点。特别是，小胶质细胞有助于调节神经炎症，具有保护和病理作用。特定的小胶质细胞激活状态不同地影响神经炎症和神经退行性疾病的进展，包括阿尔茨海默病、帕金森病、多发性硬化症和肌萎缩侧索硬化症。重要的证据表明，肠道微生物衍生的产物在整个生命周期中调节小胶质细胞的功能并影响血脑屏障。髓过氧化物酶（MPO）催化过氧化氢和氯离子转化为次氯酸，次氯酸是一种强效氧化剂，与氧化组织损伤和炎症信号调节有关。中枢神经系统中MPO水平升高与人类疾病相关，小胶质细胞中MPO活性的失调尤其有害，因为它放大了氧化应激，破坏了血脑屏障的完整性，并通过激活NF-κB等转录因子增强了神经炎症级联反应。通过选择性抑制剂或抗氧化策略靶向MPO活性可能会减弱小胶质细胞的激活并减少神经炎症，突出其作为治疗靶点的潜力，但MPO在小胶质细胞中表达的调控机制及其与其他炎症介质的相互作用仍然知之甚少。对肠道微生物群、小胶质细胞、MPO和神经炎症之间关系的新研究对于揭示神经退行性疾病以外各种情况下神经病理学的复杂性至关重要。

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引用次数: 0

Antiviral responses in peripheral and brain neurons 外周和脑神经细胞的抗病毒反应。

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-12-01 Epub Date: 2025-10-14 DOI: 10.1016/j.coi.2025.102678

Brian Imbiakha , Hana Janova , Michael S Diamond

Neurotropic viruses represent a public health challenge due to their ability to cause severe neurological conditions, including meningitis, encephalitis, and paralysis. Although many studies have investigated the immune responses to viral infections in the brain and other nervous system targets, most have focused on the effects of resident cells, such as microglia and astrocytes, and infiltrating immune cells, including neutrophils, monocytes, and T cells. However, emerging evidence has demonstrated that neurons themselves mount antiviral responses that suppress viral replication directly and enhance the inhibitory functions of adjacent glial and infiltrating immune cells. In this review, we discuss the intrinsic and extrinsic antiviral responses of neurons, highlighting mechanisms by which they detect viruses and initiate inhibitory responses to protect the nervous system from viral invasion and injury.

嗜神经病毒由于能够引起严重的神经系统疾病，包括脑膜炎、脑炎和瘫痪，对公共卫生构成挑战。尽管许多研究已经调查了大脑和其他神经系统靶点对病毒感染的免疫反应，但大多数研究都集中在驻留细胞（如小胶质细胞和星形胶质细胞）和浸润免疫细胞（包括中性粒细胞、单核细胞和T细胞）的作用上。然而，新出现的证据表明，神经元自身产生抗病毒反应，直接抑制病毒复制，增强邻近胶质细胞和浸润性免疫细胞的抑制功能。在这篇综述中，我们讨论了神经元的内在和外在抗病毒反应，重点介绍了它们检测病毒并启动抑制反应以保护神经系统免受病毒入侵和损伤的机制。

引用次数: 0

Protective or pathogenic? Tuft cells shape divergent immune outcomes in helminth and viral infections 保护性还是致病性？簇状细胞在蠕虫和病毒感染中形成不同的免疫结果

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-12-01 Epub Date: 2025-09-12 DOI: 10.1016/j.coi.2025.102657

Miles DW Tyner , Michael R Howitt

Tuft cells are epithelial sentinels that monitor the luminal environment at barrier sites throughout the body. Their function as crucial initiators of type 2 immunity against helminths and protists in the intestine emerged nearly a decade ago. Since then, key tuft cell mechanisms and effectors involved in anti-helminth immunity have been described, but their responses to a wider array of microbes, like viruses, remain far less understood. Here, we review the roles of tuft cells during both helminth and viral infections at barrier tissues like the lung and the gut. While tuft cells protect against parasite infections, they exhibit a wider and sometimes contradictory influence on viral infections and pathology. We explore the emerging and context-dependent role of tuft cells in antiviral responses and examine how tuft cells act as molecular switches during helminth–viral co-infections to dramatically alter infection outcomes.

簇状细胞是上皮哨兵，监测全身屏障部位的腔内环境。近十年前，它们作为肠道中针对蠕虫和原生生物的2型免疫的关键启动物的功能出现了。从那时起，人们已经描述了抗蠕虫免疫的关键簇毛细胞机制和效应物，但它们对更广泛的微生物（如病毒）的反应仍然知之甚少。在这里，我们回顾了簇状细胞在肺和肠道等屏障组织的蠕虫和病毒感染中的作用。虽然簇状细胞可以防止寄生虫感染，但它们对病毒感染和病理表现出更广泛的、有时是相互矛盾的影响。我们探索了簇毛细胞在抗病毒反应中的新兴和环境依赖性作用，并研究了簇毛细胞在蠕虫-病毒共感染过程中如何作为分子开关，从而显著改变感染结果。

引用次数: 0

Human inborn errors of type I interferon–independent intrinsic immunity in nonleukocytic cells 非白细胞细胞I型干扰素非依赖性固有免疫的先天性错误

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-12-01 Epub Date: 2025-09-02 DOI: 10.1016/j.coi.2025.102651

Shen-Ying Zhang , Jean-Laurent Casanova , András N Spaan

‘Intrinsic immunity’ is often used to refer to mechanisms of host defense operating in nonleukocytic cells. This term can refer to the intrinsic capacity of an individual cell to fend off invading microbes without help from other cells or of a group of similar cells to fend off invading microbes without help from other cell types. The intrinsic capacity of individual cells to defend themselves against invading microbes without assistance has received little attention and is the topic of this review. We also focus on nonleukocytic cells and on humans, the only species in which intrinsic immunity has been shown by genetic means to be essential for homeostasis in natural conditions at whole-body level. We review recent progress in our understanding of the type I interferon–independent intrinsic immunity of individual nonleukocytic cells, as inferred from human inborn errors of intrinsic immunity manifesting as infection or autoinflammation.

“内在免疫”常被用来指非白细胞细胞的宿主防御机制。这个术语可以指单个细胞在没有其他细胞帮助的情况下抵御入侵微生物的内在能力，也可以指一组类似的细胞在没有其他细胞类型帮助的情况下抵御入侵微生物的内在能力。单个细胞在没有帮助的情况下防御入侵微生物的内在能力很少受到关注，这是本综述的主题。我们还关注非白细胞细胞和人类，人类是唯一一个通过遗传手段证明内在免疫对自然条件下全身水平的稳态至关重要的物种。我们回顾了我们对个体非白细胞细胞的I型干扰素非依赖性内在免疫的理解的最新进展，从人类先天性的内在免疫错误中推断，表现为感染或自身炎症。

引用次数: 0

Treating sarcoidosis: when less is more 治疗结节病：少即是多。

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-12-01 Epub Date: 2025-10-13 DOI: 10.1016/j.coi.2025.102679

Niamh Logan , Jessica Raja , Elisabetta A Renzoni

Sarcoidosis is a heterogeneous condition, with some presentations associated with spontaneous remission and favourable outcome without treatment. Other presentations, including small fibre neuropathy, arthropathy and sarcoid-associated fatigue, can cause disabling symptoms that may not respond to disease-modifying therapies and must be managed with symptom-based treatments. Sarcoidosis can also present with organ- or life-threatening manifestations, which must be managed with disease-modifying therapies. Glucocorticoids have traditionally been used as first-line therapy, although a recent randomised controlled trial has suggested that methotrexate as sole therapy may be equally effective in pulmonary sarcoidosis, although with delayed efficacy. Growing evidence of glucocorticoid-related toxicities in sarcoid patients is prompting a paradigm shift in treatment towards a ‘less is more’ approach. In this review article, we will outline the current treatment of sarcoidosis with a particular focus on the shift away from the use of prolonged high-dose steroids.

结节病是一种异质性疾病，一些症状与自发缓解和不经治疗的良好结果有关。其他表现，包括小纤维神经病变、关节病和结节相关疲劳，可引起致残症状，这些症状可能对改善疾病的治疗无效，必须采用基于症状的治疗。结节病也可以表现为器官或危及生命的表现，这必须通过改善疾病的治疗来管理。糖皮质激素传统上被用作一线治疗，尽管最近的一项随机对照试验表明，甲氨蝶呤作为单独治疗肺结节病可能同样有效，尽管疗效延迟。越来越多的证据表明，在肉瘤患者中糖皮质激素相关的毒性正在促使治疗范式转向“少即是多”的方法。在这篇综述文章中，我们将概述目前结节病的治疗方法，特别侧重于长期使用高剂量类固醇的转变。

引用次数: 0

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