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Bacterial immunomodulatory structures as determinants of the maternal immune response and autism risk 细菌免疫调节结构作为母体免疫反应和自闭症风险的决定因素

IF 11.8 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Cytokine & Growth Factor Reviews

Pub Date : 2026-01-02 DOI: 10.1016/j.cytogfr.2025.12.010

Isaac S.B. Russell , Melissa L. Perreault

Autism is a group of neurodevelopmental conditions that have shown increasing prevalence over the last several decades. Despite being largely idiopathic in origin, numerous genetic and environmental risk factors have been identified. One of the leading environmental risk factors for autism is maternal immune activation (MIA) following infection. The impact of bacterial infection on MIA and neurodevelopmental outcomes has been widely studied though the specific causal underpinnings that directly influence autism risk remains elusive. In preclinical research, bacterial-derived lipopolysaccharide (LPS) is most often used to model bacterial infection and drive immune responses and autism-like outcomes. However, pathogenic structural determinants of the specific MIA response are rarely considered. Male and female fetuses also have distinct immune responses to MIA, which have been linked to sex-specific alterations in mitochondrial dysfunction and placental barrier disruption resulting in distinct behavioural characteristics. This review will discuss the known clinical and preclinical research on the impact of infection on MIA and neurodevelopmental outcomes, emphasizing the key role of bacterial structural factors. Here, we put forth that it is not only the severity, timing, and physical location of a bacterial infection that is important. Rather it is more nuanced, involving variations in key pathogenic immunostimulatory structures that, in turn, lead to a diversity of immune response phenotypes in both the mother and offspring, and distinct alterations in placental barrier integrity.

自闭症是一组神经发育疾病，在过去的几十年里越来越普遍。尽管在很大程度上是特发性的起源，许多遗传和环境风险因素已经确定。自闭症的主要环境风险因素之一是感染后的母体免疫激活（MIA）。细菌感染对MIA和神经发育结果的影响已经被广泛研究，尽管直接影响自闭症风险的具体因果基础仍然难以捉摸。在临床前研究中，细菌衍生的脂多糖（LPS）最常用于模拟细菌感染，驱动免疫反应和自闭症样结果。然而，很少考虑特异性MIA反应的致病结构决定因素。男性和女性胎儿对MIA也有不同的免疫反应，这与线粒体功能障碍和胎盘屏障破坏的性别特异性改变有关，从而导致不同的行为特征。本文将讨论感染对MIA和神经发育结局影响的已知临床和临床前研究，强调细菌结构因素的关键作用。在这里，我们提出，重要的不仅仅是细菌感染的严重程度、时间和物理位置。相反，它更微妙，涉及关键致病免疫刺激结构的变化，进而导致母亲和后代免疫反应表型的多样性，以及胎盘屏障完整性的明显改变。

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引用次数: 0

Missing the pattern: Pathogenic structural considerations in the maternal immune signature and autism risk 缺失模式：母体免疫特征和自闭症风险中的致病结构因素

IF 11.8 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Cytokine & Growth Factor Reviews

Pub Date : 2025-12-31 DOI: 10.1016/j.cytogfr.2025.12.011

Isaac S.B. Russell , Melissa L. Perreault

引用次数: 0

The cytokine–skin barrier axis in health and disease 健康和疾病中的细胞因子-皮肤屏障轴。

IF 11.8 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Cytokine & Growth Factor Reviews

Pub Date : 2025-12-18 DOI: 10.1016/j.cytogfr.2025.12.009

Maria Victoria Souto-Silva , Elizabete Cristina Iseke Bispo , Nakaly Natiely de Oliveira , Robert Pogue , Alessandra Zonari , Felipe Saldanha-Araujo , Juliana Lott Carvalho

The skin barrier functions as both a structural defense and an immunological interface that integrates environmental, microbial, and systemic signals. Its disruption predisposes to cutaneous inflammation and contributes to systemic immune dysregulation. In this review, we provide an integrated analysis of how cytokine signaling regulates skin barrier integrity, highlighting both mechanistic insights and clinical implications across health and disease. We first revisit the architecture of the skin barrier and describe common insults that compromise its function, and the mechanisms by which these activate canonical signalling pathways—NF-κB, MAPK, JAK-STAT, and PI3K/Akt/mTOR—leading to the release of cytokines from keratinocytes and immune cells. Particular attention is given to cytokine families with direct relevance for epidermal physiology: IL-1 and IL-17 in antimicrobial defense and hyperinflammation; IL-20, IL-31, and type 2 cytokines in keratinocyte proliferation, differentiation, and barrier protein suppression; and TNF and interferons in amplifying inflammation and tissue injury. We also discuss how these cytokine networks drive systemic manifestations, linking skin barrier dysfunction to atopic dermatitis (AD), psoriasis, inflammaging, and metabolic disorders. Finally, we review therapeutic approaches that target cytokine signaling or restore barrier integrity, ranging from emollients and microbiome-based strategies to biologics and JAK inhibitors. By systematically reviewing the cytokine–barrier axis, this work highlights how modulation of cytokine signaling represents a promising avenue for clinical and preventive interventions in dermatology and systemic health.

皮肤屏障的功能既是结构防御，也是整合环境、微生物和系统信号的免疫界面。它的破坏容易引起皮肤炎症，并导致全身免疫失调。在这篇综述中，我们提供了细胞因子信号如何调节皮肤屏障完整性的综合分析，强调了在健康和疾病方面的机制见解和临床意义。我们首先回顾了皮肤屏障的结构，并描述了损害其功能的常见损伤，以及这些损伤激活典型信号通路（nf -κB、MAPK、JAK-STAT和PI3K/Akt/ mtor）的机制，这些信号通路导致角质形成细胞和免疫细胞释放细胞因子。特别关注与表皮生理学直接相关的细胞因子家族：IL-1和IL-17在抗菌防御和高炎症；IL-20、IL-31和2型细胞因子在角质形成细胞增殖、分化和屏障蛋白抑制中的作用TNF和干扰素对炎症和组织损伤的影响。我们还讨论了这些细胞因子网络如何驱动全身表现，将皮肤屏障功能障碍与特应性皮炎（AD）、牛皮癣、炎症和代谢紊乱联系起来。最后，我们回顾了针对细胞因子信号传导或恢复屏障完整性的治疗方法，从润润剂和基于微生物组的策略到生物制剂和JAK抑制剂。通过系统地回顾细胞因子-屏障轴，这项工作强调了细胞因子信号的调节如何代表了皮肤病和全身健康的临床和预防性干预的有前途的途径。

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引用次数: 0

Interferons as therapeutic orchestrators of cancer stem cell plasticity and therapy response 干扰素作为肿瘤干细胞可塑性和治疗反应的治疗协调者

IF 11.8 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Cytokine & Growth Factor Reviews

Pub Date : 2025-12-15 DOI: 10.1016/j.cytogfr.2025.12.008

Deepakshi Kasat , Sophia Hidalgo , Lu Wang, Jack D Bui, Magalie Dosset

Cancer stem cells (CSCs) represent a small but critical subset of tumor cells characterized by their inherent self-renewal ability, differentiation potential, and resistance to cancer therapies. Their capacity to reversibly transition between a stem-like and differentiated state, together with their ability to enter into quiescence, are key determinants of their contribution to tumor initiation, tumor progression, metastasis, and cancer recurrence. Among the various factors in the tumor microenvironment, increasing evidence suggests that interferons (IFNs) are key extrinsic modulators of CSC fate. Although type I (IFN-α/β) and type II (IFN-γ) IFNs have long been recognized for their antitumor properties, recent studies indicate that IFN-signaling may also facilitate CSC induction and maintenance. In this review, we summarize and critically assess our current understanding of the complex roles of IFNs in governing CSC survival, plasticity, and immunogenicity. We discuss how IFN-signaling thresholds, signaling duration, and intrinsic CSC regulatory networks determine whether IFNs suppress CSCs or instead reinforce stemness. By bridging mechanistic insights with therapeutic potential and clinical outcomes, we highlight emerging opportunities to exploit IFN pathways for improved biomarkers and therapeutic strategies to overcome CSC-driven resistance.

肿瘤干细胞（CSCs）是肿瘤细胞中一个小而关键的子集，其特点是具有固有的自我更新能力、分化潜力和对癌症治疗的抵抗力。它们在干细胞样状态和分化状态之间可逆转换的能力，以及它们进入静止状态的能力，是它们对肿瘤起始、肿瘤进展、转移和癌症复发的关键决定因素。在肿瘤微环境中的各种因素中，越来越多的证据表明干扰素（ifn）是影响CSC命运的关键外源性调节剂。虽然I型（IFN-α/β）和II型（IFN-γ） IFN长期以来被认为具有抗肿瘤特性，但最近的研究表明IFN信号传导也可能促进CSC的诱导和维持。在这篇综述中，我们总结并批判性地评估了我们目前对ifn在控制CSC存活、可塑性和免疫原性中的复杂作用的理解。我们讨论了ifn信号阈值、信号持续时间和内在的CSC调节网络如何决定ifn是抑制CSC还是增强干细胞。通过将机制与治疗潜力和临床结果联系起来，我们强调了利用IFN途径改善生物标志物和治疗策略以克服csc驱动的耐药性的新机会。

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引用次数: 0

Tightly bound T-cell clusters: A new class of hyper-effector tumor killers 紧密结合的t细胞簇：一类新的超效应肿瘤杀手。

IF 11.8 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Cytokine & Growth Factor Reviews

Pub Date : 2025-12-13 DOI: 10.1016/j.cytogfr.2025.12.007

Wenxue Ma, Jessica Pham, Catriona Jamieson

T cells have traditionally been characterized as autonomous killers that eliminate malignant cells through single-cell cytotoxicity. However, recent findings reveal that tumor-reactive T cells frequently form tightly bound clusters on the tumor surface, functioning as cooperative hyper-effector units. These clusters establish stable and reinforced immune synapses, sustain prolonged engagement with tumor targets, and coordinate the delivery of perforin, granzymes, and proinflammatory cytokines. As a result, they exhibit markedly enhanced tumor-killing capacity compared with unbound T cells in both ex vivo assays and murine models. This discovery introduces an essential spatial and mechanical dimension to cancer immunology and challenges the prevailing assumption that molecular phenotype alone defines T-cell efficacy. The implications are substantial, extending to tumor-infiltrating lymphocyte (TIL) therapy optimization, the refinement of immunotherapy biomarkers, and the engineering of next-generation CAR-T and CAR-NK platforms. Enriching or mimicking the behavior of cluster-forming T cells may accelerate clinical responses and overcome barriers associated with solid tumors. Collectively, these insights reposition T-cell clustering as a fundamental determinant of effective antitumor immunity.

传统上，T细胞被认为是通过单细胞毒性消除恶性细胞的自主杀手。然而，最近的研究结果表明，肿瘤反应性T细胞经常在肿瘤表面形成紧密结合的簇，作为协同的超效应单位发挥作用。这些团簇建立稳定和增强的免疫突触，维持与肿瘤靶点的长期接触，并协调穿孔素、颗粒酶和促炎细胞因子的传递。结果，在离体实验和小鼠模型中，与未结合的T细胞相比，它们表现出明显增强的肿瘤杀伤能力。这一发现为癌症免疫学引入了一个重要的空间和机械维度，并挑战了分子表型单独定义t细胞功效的普遍假设。这项研究的意义是重大的，可以扩展到肿瘤浸润性淋巴细胞（TIL）治疗的优化、免疫治疗生物标志物的改进以及下一代CAR-T和CAR-NK平台的设计。富集或模拟簇状T细胞的行为可能会加速临床反应并克服与实体瘤相关的障碍。总的来说，这些见解将t细胞聚集重新定位为有效抗肿瘤免疫的基本决定因素。

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引用次数: 0

Combination therapy strategies targeting glypican-3 in hepatocellular carcinoma: A comprehensive review 针对glypican-3的肝细胞癌联合治疗策略：综合综述。

IF 11.8 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Cytokine & Growth Factor Reviews

Pub Date : 2025-12-12 DOI: 10.1016/j.cytogfr.2025.12.006

Sina Nabiyi , Mohammad Heiat , Ehsan Rezaei

Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide. Advanced disease often proves resistant to conventional therapies, thereby driving the intensive search for targeted therapies. Glypican-3 (GPC3), a well-validated, signature tumor antigen in HCC, has emerged as an attractive therapeutic target with high potential for precision oncology. Current research strategies for developing novel GPC3-targeted therapeutics are highly diverse, encompassing cellular immunotherapies (e.g., CAR-T and NK cell therapies), antibody-based agents, immunotoxins, peptide vaccines, gene therapies, and nanoparticle-mediated drug delivery systems. Despite promising preclinical and clinical developments, the clinical translation of GPC3-targeted therapies is limited by challenges such as inadequate tumor penetration, immunosuppressive tumor microenvironment, and heterogeneous antigen expression. Consequently, recent research has increasingly shifted toward combination strategies. A growing body of experimental and early clinical data indicates that GPC3-targeted agents synergize effectively with a broad range of co-treatments, including immune checkpoint inhibitors, antiangiogenics, immune modulators, tyrosine kinase inhibitors, radiotherapy, chemotherapy, and local therapies to enhance antitumoral efficacy. In this review, we examine the potential of these multimodal strategies to develop more effective therapeutic approaches for HCC. Future studies should therefore focus on optimizing these combination regimens by incorporating personalized treatment strategies to achieve durable clinical outcomes.

肝细胞癌（HCC）仍然是世界范围内癌症相关死亡的主要原因。晚期疾病往往证明对常规疗法有抗药性，因此推动了对靶向疗法的密集研究。Glypican-3 （GPC3）是HCC中一种经过充分验证的标志性肿瘤抗原，已成为一种具有高潜力的精准肿瘤学治疗靶点。目前开发新型gpc3靶向疗法的研究策略非常多样化，包括细胞免疫疗法（例如，CAR-T和NK细胞疗法）、基于抗体的药物、免疫毒素、肽疫苗、基因疗法和纳米颗粒介导的药物递送系统。尽管临床前和临床发展前景良好，但gpc3靶向治疗的临床转化受到诸如肿瘤渗透不足、免疫抑制肿瘤微环境和异质抗原表达等挑战的限制。因此，最近的研究越来越多地转向组合策略。越来越多的实验和早期临床数据表明，gpc3靶向药物与广泛的联合治疗有效协同，包括免疫检查点抑制剂、抗血管生成、免疫调节剂、酪氨酸激酶抑制剂、放疗、化疗和局部治疗，以增强抗肿瘤疗效。在这篇综述中，我们研究了这些多模式策略的潜力，以开发更有效的HCC治疗方法。因此，未来的研究应侧重于通过结合个性化治疗策略来优化这些联合方案，以获得持久的临床结果。

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引用次数: 0

Emerging involvement of CXCL13 in cancer development and progression 新发现的CXCL13参与癌症的发生和发展

IF 11.8 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Cytokine & Growth Factor Reviews

Pub Date : 2025-12-11 DOI: 10.1016/j.cytogfr.2025.12.005

Dimitrios G. Argyris , Lillian Johnson , Thomas Hägglöf , Panagiota S. Filippou , George S. Karagiannis

CXCL13, a chemokine originally identified for its role in B-cell trafficking, signals through the G-protein-coupled receptor CXCR5, to organize germinal centers and maintain immune architecture in secondary lymphoid organs. Beyond its physiological functions, accumulating evidence implicates the CXCL13-CXCR5 axis in the reciprocal regulation of inflammation and cancer. In this review, we outline our current understanding of its molecular organization, signaling properties, and regulatory feedback loops that fine-tune receptor activity. We further examine how CXCL13-CXCR5 signaling contributes to aquisition of cancer hallmarks, mainly through angiogenesis, epithelial-mesenchymal transition, metastatic niche conditioning, and the formation of tertiary lymphoid structures that influence antitumor immunity. By integrating biochemical, structural, and immunological insights, this review highlights the CXCL13-CXCR5 axis as a critical interface between lymphoid neogenesis and tumor evolution, and as a potential target for therapeutic modulation in cancer.

CXCL13是一种趋化因子，最初被发现在b细胞运输中起作用，通过g蛋白偶联受体CXCR5发出信号，组织生发中心并维持次级淋巴器官的免疫结构。除了其生理功能外，越来越多的证据表明CXCL13-CXCR5轴在炎症和癌症的相互调节中起作用。在这篇综述中，我们概述了我们目前对其分子组织、信号特性和调节受体活性的调节反馈回路的理解。我们进一步研究了CXCL13-CXCR5信号通路如何通过血管生成、上皮-间质转化、转移生态位调节和影响抗肿瘤免疫的三级淋巴结构的形成来促进癌症特征的获得。通过整合生化、结构和免疫学的见解，本综述强调了CXCL13-CXCR5轴是淋巴细胞新生和肿瘤进化之间的关键接口，也是癌症治疗调节的潜在靶点。

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引用次数: 0

Role of anti-tumorigenic cytokines in gastrointestinal cancers 抗肿瘤细胞因子在胃肠道肿瘤中的作用。

IF 11.8 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Cytokine & Growth Factor Reviews

Pub Date : 2025-12-06 DOI: 10.1016/j.cytogfr.2025.12.004

Olivia Hooks , Lily T. Childers , Justin T. Childers , Christopher Machado , Colton C. Mowers , Sarfraz Ahmad

Gastrointestinal (GI) cancers are among the deadliest worldwide, with millions of cases and deaths annually. In the U.S., they account for over 25 % of cancer-related deaths, with colorectal cancer (CRC) leading in incidence and mortality, followed by pancreatic, liver, gastric, and esophageal cancers. These malignancies vary in cellular origin and etiology but share common risk factors, which contribute to chronic inflammation and immune dysfunction, influencing cytokine-driven pathways that shape the tumor environment. This review outlines and discusses the anti-tumorigenic properties of key/select cytokines such as interleukin (IL)-12, IL-15, IL-2, and interferon (IFN)-γ with recent discoveries, therapeutic advancements, and persistent challenges in cytokine biology for GI cancers. We searched with keywords for articles published in the last 20 years. IL-12, IL-15, IL-2, and IFN-γ all regulate or promote natural killer (NK)-cells and T-lymphocytes to suppress GI tumor growth. When deleted in tumor models, there is an increase in other inflammatory mediators that result in cancer progression. The literature supports an inverse relationship between low cytokine levels and advanced-stage disease. While the literature suggests these cytokines are not as beneficial or potentially harmful as single agents, when used in GI cancer treatment as an adjuvant in combination therapies or with innovative delivery methods, there is statistically significant therapeutic efficacy with improved clinical outcomes, median survival, and tumor suppression. The applicability of anti-tumorigenic cytokines (IL-12, IL-15, IL-2, and IFN-γ) as biomarkers of diagnosis and indicators of prognosis is being recognized with emphasis on their capabilities as therapeutic targets and adjuvant therapies in GI cancers.

胃肠道（GI）癌症是世界上最致命的癌症之一，每年有数百万病例和死亡。在美国，它们占癌症相关死亡人数的25% %以上，其中结直肠癌（CRC）的发病率和死亡率最高，其次是胰腺癌、肝癌、胃癌和食管癌。这些恶性肿瘤在细胞起源和病因上各不相同，但具有共同的危险因素，这些因素有助于慢性炎症和免疫功能障碍，影响塑造肿瘤环境的细胞因子驱动途径。本文概述并讨论了关键/选择细胞因子如白细胞介素(IL)-12、IL-15、IL-2和干扰素(IFN)-γ的抗肿瘤特性，以及GI癌症细胞因子生物学的最新发现、治疗进展和持续挑战。我们用关键词搜索近20年发表的文章。IL-12、IL-15、IL-2和IFN-γ均可调节或促进自然杀伤细胞（NK）和t淋巴细胞抑制胃肠道肿瘤生长。当在肿瘤模型中删除时，导致癌症进展的其他炎症介质增加。文献支持低细胞因子水平与晚期疾病之间的反比关系。虽然文献表明这些细胞因子不像单一药物那样有益或潜在有害，但当用于胃肠道癌症治疗时，作为联合治疗的辅助治疗或与创新的给药方法一起使用，具有统计学上显著的治疗效果，改善了临床结果、中位生存期和肿瘤抑制。抗肿瘤细胞因子（IL-12、IL-15、IL-2和IFN-γ）作为诊断和预后指标的适用性正在得到认可，重点是它们作为GI癌症的治疗靶点和辅助治疗的能力。

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引用次数: 0

Meteorin-like/Metrnl: A pleiotropic cytokine implicated in metabolic, inflammatory and malignant disorders 流星蛋白样/Metrnl：一种多效细胞因子，与代谢、炎症和恶性疾病有关。

IF 11.8 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Cytokine & Growth Factor Reviews

Pub Date : 2025-12-05 DOI: 10.1016/j.cytogfr.2025.12.003

Jinlian Li , Pei Ye , Jingli Si , Guangda Xiang

Metrnl, a secreted protein highly expressed in adipocytes, endothelial cells, muscle cells, and activated macrophages, has been identified as a novel myokine and adipokine. It plays important roles in enhancing white fat browning, improving insulin sensitivity, modulating glucose homeostasis and regulating inflammatory response. These studies suggest that Metrnl could be a promising biomarker and a potential therapeutic target for the related diseases. However, it is worth noting that there are still several controversies persist within its research field: 1. Metrnl concentrations in patients with type 2 diabetes and obesity yield conflicting results, which has raised doubts about the precise role and reliable application of Metrnl as a biomarker in metabolic diseases; 2. Metrnl exhibits a dual nature that is dependent on specific environments, with both anti-inflammatory and proinflammatory functions; 3.Exercise-induced Metrnl can bring about systemic metabolic benefits, but the CD8⁺ T cell -derived Metrnl impairs anti-tumor effects, raising a critical concern about the potential effects of exercise-induced Metrnl on cancer progression. Therefore, this review would explore those significant controversies and conflicting results surrounding the function and clinical relevance of Metrnl, and proposes future research directions to utilize the therapeutic potential of Metrnl in metabolic and inflammatory and malignant disorders.

Metrnl是一种在脂肪细胞、内皮细胞、肌肉细胞和活化的巨噬细胞中高度表达的分泌蛋白，已被确定为一种新的肌因子和脂肪因子。它在促进白色脂肪褐变、改善胰岛素敏感性、调节葡萄糖稳态和调节炎症反应等方面发挥重要作用。这些研究表明，Metrnl可能是一个有前景的生物标志物和潜在的治疗相关疾病的靶点。然而，值得注意的是，在其研究领域中仍存在一些争议：1。2型糖尿病和肥胖症患者的Metrnl浓度产生相互矛盾的结果，这引起了对Metrnl作为代谢性疾病生物标志物的确切作用和可靠应用的质疑；2. Metrnl表现出依赖于特定环境的双重性质，具有抗炎和促炎功能；3.运动诱导的Metrnl可以带来全身代谢益处，但CD8+ T细胞衍生的Metrnl会损害抗肿瘤作用，这引起了人们对运动诱导的Metrnl对癌症进展的潜在影响的关注。因此，本文将探讨围绕Metrnl的功能和临床相关性的重大争议和相互矛盾的结果，并提出未来的研究方向，以利用Metrnl在代谢、炎症和恶性疾病中的治疗潜力。

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引用次数: 0

Post COVID-19 pandemic Inflammatory Insights into Cancer: Consequences for immunotherapy COVID-19大流行后对癌症的炎症洞察：免疫治疗的后果。

IF 11.8 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Cytokine & Growth Factor Reviews

Pub Date : 2025-12-03 DOI: 10.1016/j.cytogfr.2025.12.002

Carla Eksteen , Lé-chandré Asja , Atarah Rass , Johann Riedemann , Anna-Mart Engelbrecht

The COVID-19 pandemic has reshaped the landscape of global health, revealing novel interactions between infectious diseases and chronic conditions such as cancer. Beyond acute infection, growing evidence suggests that persistent exposure to SARS-CoV-2 spike protein, whether through infection or vaccination, may sustain inflammatory pathways that contribute to tumour progression and immune modulation. This review explores the overlap between post-COVID inflammation, particularly in Long-COVID syndromes and the tumour microenvironment (TME), focusing on key mediators such as IL-6, TNF-α, IL-1β, and NF-κB. We revisit the concept of the cytokine storm in the context of persistent inflammation, spike protein immunogenicity and immune exhaustion, proposing a model in which chronic inflammatory signalling may disrupt tumour immune surveillance, reawaken dormant cancer cells and compromise the efficacy of immunotherapies. Comparative analysis with other cancer types highlights shared pathways of oncogenic inflammation. Lastly, we outline emerging therapeutic strategies to mitigate these effects, including cytokine-targeted interventions and immunomodulatory screening in post-COVID cancer patients. These post-pandemic insights call for urgent translational research to ensure effective and safe cancer immunotherapy in the evolving inflammatory landscape.

2019冠状病毒病大流行重塑了全球卫生格局，揭示了传染病与癌症等慢性病之间新的相互作用。除了急性感染之外，越来越多的证据表明，无论是通过感染还是通过疫苗接种，持续暴露于SARS-CoV-2刺突蛋白都可能维持炎症途径，从而促进肿瘤进展和免疫调节。本文探讨了covid后炎症，特别是长covid综合征与肿瘤微环境（TME）之间的重叠，重点关注IL-6、TNF-α、IL-1β和NF-κB等关键介质。我们在持续炎症、刺突蛋白免疫原性和免疫衰竭的背景下重新审视了细胞因子风暴的概念，提出了一种慢性炎症信号可能破坏肿瘤免疫监视、重新唤醒休眠癌细胞并损害免疫治疗效果的模型。与其他癌症类型的比较分析强调了致癌炎症的共同途径。最后，我们概述了减轻这些影响的新兴治疗策略，包括细胞因子靶向干预和covid后癌症患者的免疫调节筛查。这些大流行后的见解要求进行紧急的转化研究，以确保在不断变化的炎症环境中有效和安全的癌症免疫治疗。

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引用次数: 0