Seminars in Immunology最新文献_第5页

Interplay between the complement system and other immune pathways in the tumor microenvironment 肿瘤微环境中补体系统与其他免疫途径的相互作用

IF 7.4 2区医学 Q1 IMMUNOLOGY

Seminars in Immunology

Pub Date : 2025-04-09 DOI: 10.1016/j.smim.2025.101951

Cecilia Garlanda , Monica Dambra , Elena Magrini

Tumor growth and spread are sustained by the tumor microenvironment. Inflammatory cells and pathways have a fundamental role in the tumor microenvironment, driving or conditioning the functional activation of other leukocyte subsets and favoring evasion of anti-tumor immunity. One of the inflammatory pathways contributing to cancer-related inflammation is the complement system. Complement has long been considered an immune mechanism associated with immunosurveillance. More recently it emerged as a tumor promoting pathway, due to direct effects on cancer cells or indirect effects via immunosuppression driven by myeloid cells. The role of complement in cancer is complex and ambiguous, and depends on the tumor type and stage, as well as other factors including oncogenic drivers, leukocyte infiltration, interactions with other tumor microenvironment components or tumor cells. Other factors of complexity include the source of complement molecules, its canonical or non-canonical extracellular functions, its potential intracellular activation, and the interaction with other systems, such as the coagulation or the microbiome. Preclinical studies generally demonstrate the involvement of complement activation in smouldering inflammation in cancer and promotion of an immunosuppressive environment. These studies paved the way for clinical trials aimed at enhancing the potential of immunotherapy, in particular by targeting complement-dependent myeloid-sustained immunosuppression. However, the complex role of complement in cancer and the multiplicity of complement players may represent stumbling blocks and account for failures of clinical trials, and suggest that further studies are required to identify patient subsets who may benefit from specific complement molecule targeting in combination with conventional therapies or immunotherapy. Here, we will discuss the anti- or pro-tumor role of complement activation in cancer, focusing on the interactions of complement with immune cells within the tumor microenvironment, in particular the myeloid compartment. Furthermore, we will examine the potential of complement targeting in cancer treatment, particularly in the context of macrophage reprogramming.

肿瘤的生长和扩散是由肿瘤微环境维持的。炎症细胞和途径在肿瘤微环境中起着重要作用，驱动或调节其他白细胞亚群的功能激活，并有利于逃避抗肿瘤免疫。导致癌症相关炎症的炎症途径之一是补体系统。补体一直被认为是一种与免疫监视相关的免疫机制。最近，由于直接作用于癌细胞或通过骨髓细胞驱动的免疫抑制间接作用，它成为一种促进肿瘤的途径。补体在癌症中的作用是复杂而模糊的，取决于肿瘤的类型和分期，以及其他因素，包括致癌驱动因素、白细胞浸润、与其他肿瘤微环境成分或肿瘤细胞的相互作用。其他复杂因素包括补体分子的来源，其典型或非典型的细胞外功能，其潜在的细胞内激活，以及与其他系统的相互作用，如凝血或微生物组。临床前研究普遍表明，补体激活参与了癌症的阴燃炎症和促进免疫抑制环境。这些研究为旨在增强免疫治疗潜力的临床试验铺平了道路，特别是通过靶向补体依赖性骨髓持续免疫抑制。然而，补体在癌症中的复杂作用和补体参与者的多样性可能是临床试验失败的绊脚石，并表明需要进一步的研究来确定可能从特异性补体分子靶向与常规疗法或免疫疗法联合中受益的患者亚群。在这里，我们将讨论补体激活在癌症中的抗或促肿瘤作用，重点是补体与肿瘤微环境中免疫细胞的相互作用，特别是髓细胞室。此外，我们将研究补体靶向在癌症治疗中的潜力，特别是在巨噬细胞重编程的背景下。

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引用次数: 0

Endogenous glucocorticoids and human immunity: Time to revisit old dogmas 内源性糖皮质激素和人体免疫：是时候重新审视旧教条了

IF 7.4 2区医学 Q1 IMMUNOLOGY

Seminars in Immunology

Pub Date : 2025-04-08 DOI: 10.1016/j.smim.2025.101949

Brinda Bhatt , Luis M. Franco

Glucocorticoids (GCs) are steroid hormones with diverse and important roles in the physiologic response to stress. These include permissive and suppressive effects on immunity, which help prepare the organism for future infectious stressors and control the immunological response to a recent stressor, preventing autoimmune damage. The ability of GCs to rapidly suppress an overactive immune system has been harnessed pharmacologically and synthetic GCs have played a central role in the treatment of inflammatory and autoimmune diseases for the past eight decades. Given their importance in clinical medicine, an emphasis on the anti-inflammatory and immunosuppressive effects of synthetic GCs has overshadowed the study of the physiologic roles of endogenous GCs in human immunity. The rising interest in the intersection between neurobiology and immunity, and the development of technologies that facilitate direct experimentation with human cells and tissues, make this an ideal time to critically review existing knowledge on this subject. In this review of the past 100 years of biomedical literature on the effects of endogenous glucocorticoids on human immunity, we summarize existing experimental evidence, reveal key knowledge gaps and misconceptions, and highlight specific areas of opportunity for new research.

糖皮质激素（GCs）是一种类固醇激素，在生理应激反应中具有多种重要作用。这些包括对免疫的允许和抑制作用，这有助于机体为未来的感染压力源做好准备，并控制对最近压力源的免疫反应，防止自身免疫损伤。在过去的80年里，GCs快速抑制过度活跃的免疫系统的能力已经被药理学利用，合成GCs在炎症和自身免疫性疾病的治疗中发挥了核心作用。鉴于其在临床医学中的重要性，对合成GCs的抗炎和免疫抑制作用的强调掩盖了对内源性GCs在人体免疫中的生理作用的研究。人们对神经生物学和免疫之间的交叉越来越感兴趣，以及促进对人类细胞和组织进行直接实验的技术的发展，使现在成为批判性地审查这一主题现有知识的理想时机。在本文中，我们回顾了过去100年来关于内源性糖皮质激素对人体免疫影响的生物医学文献，总结了现有的实验证据，揭示了关键的知识空白和误解，并强调了新研究的具体领域。

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引用次数: 0

The role of the adaptive immune system in the initiation and persistence of multiple sclerosis 适应性免疫系统在多发性硬化症的发生和持续中的作用

IF 7.4 2区医学 Q1 IMMUNOLOGY

Seminars in Immunology

Pub Date : 2025-04-02 DOI: 10.1016/j.smim.2025.101947

Ali Maisam Afzali , Thomas Korn

Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the central nervous system (CNS) in which complex networks of interacting immune cells initiate and sustain the disease. The pathogenesis of relapsing MS is driven by adaptive immune cells that become activated outside the CNS compartment and then migrate into the CNS to initiate a presumably autoimmune inflammatory process. Recent technological advances, particularly single-cell analyses, have revealed substantial heterogeneity in T and B cells involved in this stage of the disease. Disease progression involves different mechanisms, with compartmentalized inflammation and chronic activation of CNS-resident cells becoming predominant features. The contribution of tissue-resident adaptive immune cells to the pathology of progressive MS, including tissue-resident CD8⁺ T cells and B cells in the meningeal compart, is increasingly debated. Here, we will discuss concepts of how adaptive immune cells might initiate and maintain autoimmune inflammation in the CNS, while the responses to autoimmune inflammation of CNS intrinsic cells, including astrocytes, oligodendrocytes, and neurons, are described elsewhere [1], [2], [3], [4], [5] and will not be a particular focus of this overview. Finally, it is the aim of this review to conceptualize the grounds for efficient therapeutic interventions targeting players of the adaptive immune system in relapsing but also in progressive MS.

多发性硬化症（MS）是一种中枢神经系统（CNS）的炎症性脱髓鞘疾病，免疫细胞相互作用的复杂网络引发并维持了这种疾病。多发性硬化症复发的发病机制是由适应性免疫细胞驱动的，这些细胞在中枢神经系统外被激活，然后迁移到中枢神经系统，启动一个可能的自身免疫性炎症过程。最近的技术进步，特别是单细胞分析，已经揭示了参与这一阶段疾病的T细胞和B细胞的实质性异质性。疾病进展涉及不同的机制，区隔性炎症和中枢系统驻留细胞的慢性激活成为主要特征。组织常驻适应性免疫细胞在进展性MS病理中的作用，包括组织常驻CD8+ T细胞和脑膜区B细胞，越来越受到争论。在这里，我们将讨论适应性免疫细胞如何在中枢神经系统中启动和维持自身免疫性炎症的概念，而中枢神经系统固有细胞（包括星形胶质细胞、少突胶质细胞和神经元）对自身免疫性炎症的反应将在[1]、[2]、[3]、[4]、[5]中描述，这将不是本综述的特别重点。最后，这篇综述的目的是概念化针对复发性多发性硬化症和进展性多发性硬化症的适应性免疫系统参与者的有效治疗干预的基础。

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引用次数: 0

Complement and the hallmarks of cancer 补体和癌症的标志

IF 7.4 2区医学 Q1 IMMUNOLOGY

Seminars in Immunology

Pub Date : 2025-04-02 DOI: 10.1016/j.smim.2025.101950

Mikel Rezola Artero , Andrea Minery , Leon Nedelcev , Maria Radanova , Lubka T. Roumenina

The hallmarks of cancer are a set of traits that normal cells acquire during their transformation into malignancy. Among the biological processes influencing these hallmarks, the innate immune complement system plays a critical role. It can operate canonically—in blood and tissues—via phagocytosis, inflammation, and complement-dependent cytotoxicity, similar to its roles against invading pathogens. Additionally, it functions non-canonically by modulating the behavior of cells within the tumor microenvironment and their intracellular landscape which regulates cell fate. These mechanisms contribute to the complex and context-dependent roles of complement in both tumor growth and antitumor immunity, shaped by the characteristics of the dynamic tumor microenvironment. This review analyses the multifaceted interplay between complement proteins and cancer hallmarks, positioning this system as a target to cancer therapy.

癌症的特征是正常细胞在向恶性肿瘤转化过程中获得的一系列特征。在影响这些特征的生物过程中，先天免疫补体系统起着至关重要的作用。它可以在血液和组织中正常运作，通过吞噬、炎症和补体依赖性细胞毒性，类似于它抵抗入侵病原体的作用。此外，它通过调节肿瘤微环境中细胞的行为和调节细胞命运的细胞内景观而发挥非典型的作用。这些机制有助于补体在肿瘤生长和抗肿瘤免疫中的复杂和情境依赖性作用，由动态肿瘤微环境的特征决定。这篇综述分析了补体蛋白与癌症标志物之间多方面的相互作用，将该系统定位为癌症治疗的靶点。

引用次数: 0

Variable domain glycosylation as a marker and modulator of immune responses: Insights into autoimmunity and B-cell malignancies 可变结构域糖基化作为免疫反应的标志物和调节剂：对自身免疫和b细胞恶性肿瘤的见解

IF 7.4 2区医学 Q1 IMMUNOLOGY

Seminars in Immunology

Pub Date : 2025-03-29 DOI: 10.1016/j.smim.2025.101946

Roxane Biersteker , Oliver F. Larsen , Manfred Wuhrer , Tom W.J. Huizinga , René E.M. Toes , Lise Hafkenscheid

Glycosylation of antibodies is essential for shaping immune responses, as it contributes significantly to antibody function and diversity. While immunoglobulin G (IgG) Fc glycosylation is well-characterized, variable domain glycosylation (VDG) introduces an additional and less understood layer of complexity. Notably, VDG is associated with rheumatoid arthritis, where disease-specific IgG autoantibodies abundantly express this modification. Moreover, its presence on these antibodies correlates with disease progression in at-risk individuals and therapeutic outcomes. Emerging evidence links increased VDG levels to other autoimmune diseases and B-cell malignancies, highlighting its potential as both a marker and modulator in disease onset and progression. Importantly, VDG on IgG is now recognized to influence antigen binding, enhance antibody stability, and modulate interactions with the human neonatal Fc receptor. In addition, glycans in the antigen-binding domains of autoreactive B-cell receptors (BCRs) can significantly impact B cell activation. In follicular lymphoma and other B-cell malignancies, the presence of N-glycosylation sites in the immunoglobulin variable domains leads to the introduction of oligomannose glycans, which are postulated to bind to mannose-specific lectins. This interaction might promote antigen-independent activation of BCRs, thereby supporting malignant B cell survival and proliferation. Here, we explore the regulatory pathways of VDG and its functional roles across both physiological and pathological conditions, underscoring its prevalence and significance in various autoimmune diseases and B-cell malignancies. Ultimately, advancing our understanding of the regulatory factors influencing VDG and its functional implications could be highly rewarding for identifying potential therapeutic targets and strategies to prevent and treat autoimmune diseases and B-cell malignancies.

抗体的糖基化对形成免疫反应至关重要，因为它对抗体的功能和多样性有重要贡献。虽然免疫球蛋白G (IgG) Fc糖基化已被很好地表征，但可变结构域糖基化（VDG）引入了一个额外的、鲜为人知的复杂性层。值得注意的是，VDG与类风湿关节炎相关，其中疾病特异性IgG自身抗体大量表达这种修饰。此外，它在这些抗体上的存在与高危个体的疾病进展和治疗结果相关。新出现的证据表明VDG水平升高与其他自身免疫性疾病和b细胞恶性肿瘤有关，突出了其作为疾病发生和进展的标志物和调节剂的潜力。重要的是，IgG上的VDG现在被认为影响抗原结合，增强抗体稳定性，并调节与人类新生儿Fc受体的相互作用。此外，自身反应性B细胞受体（bcr）抗原结合域的聚糖可以显著影响B细胞的活化。在滤泡性淋巴瘤和其他b细胞恶性肿瘤中，免疫球蛋白可变结构域中n -糖基化位点的存在导致低甘露糖聚糖的引入，这些低甘露糖聚糖被认为与甘露糖特异性凝集素结合。这种相互作用可能促进bcr的抗原非依赖性激活，从而支持恶性B细胞的存活和增殖。在这里，我们探讨VDG的调控途径及其在生理和病理条件下的功能作用，强调其在各种自身免疫性疾病和b细胞恶性肿瘤中的患病率和意义。最终，推进我们对影响VDG的调节因子及其功能意义的理解，可能对确定预防和治疗自身免疫性疾病和b细胞恶性肿瘤的潜在治疗靶点和策略具有很高的回报。

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引用次数: 0

Interferon regulatory factor 3 beyond innate immunity: Regulation in obesity and metabolic disorders 先天免疫之外的干扰素调节因子3：肥胖和代谢紊乱的调节

IF 7.4 2区医学 Q1 IMMUNOLOGY

Seminars in Immunology

Pub Date : 2025-03-28 DOI: 10.1016/j.smim.2025.101948

Heng Li , Yongliang Zhang , Hong Yong Peh

Interferon regulatory factor 3 (IRF3) is a transcription factor known primarily for its role in antiviral immunity via regulation of type I interferons (IFNs). Recent research has broadened its significance to encompass metabolic disorders, particularly obesity and diabetes. Obesity is characterized by chronic low-grade inflammation, insulin resistance, and metabolic dysfunction, all of which are increasingly found to be associated with immune signaling pathways. IRF3 has emerged as an important regulator in the development of obesity and type 2 diabetes (T2D), predominantly through its regulation of inflammatory cytokines production in various cells in adipose tissue. In obese individuals, IRF3 is activated in the adipocytes and adipose tissue macrophages, to promote the expression of inflammatory cytokines, thereby contributing to chronic inflammation and exacerbating insulin resistance. Moreover, IRF3 has been linked to mitochondrial dysfunction in hepatic disorders, further amplifying metabolic stress and imbalances associated with obesity. The growing evidence suggests that IRF3 is an important mediator in both immune and metabolic pathways, highlighting its potential as a target for the development of therapeutic interventions for obesity-related inflammation and metabolic dysfunction.

干扰素调节因子3 （IRF3）是一种转录因子，主要通过调节I型干扰素（ifn）在抗病毒免疫中发挥作用。最近的研究扩大了它的意义，包括代谢紊乱，特别是肥胖和糖尿病。肥胖的特点是慢性低度炎症、胰岛素抵抗和代谢功能障碍，所有这些都被越来越多地发现与免疫信号通路有关。IRF3已成为肥胖和2型糖尿病（T2D）发展的重要调节因子，主要通过调节脂肪组织中各种细胞的炎症细胞因子产生。在肥胖个体中，IRF3在脂肪细胞和脂肪组织巨噬细胞中被激活，促进炎症因子的表达，从而导致慢性炎症，加剧胰岛素抵抗。此外，IRF3与肝脏疾病中的线粒体功能障碍有关，进一步放大了与肥胖相关的代谢应激和失衡。越来越多的证据表明，IRF3在免疫和代谢途径中都是一个重要的介质，这突出了它作为治疗肥胖相关炎症和代谢功能障碍的治疗干预措施的潜力。

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引用次数: 0

The immunological processes behind aquaporin 4-antibody seropositive neuromyelitis optica spectrum disorders 水通道蛋白4抗体血清阳性视神经脊髓炎谱系障碍背后的免疫学过程

IF 7.4 2区医学 Q1 IMMUNOLOGY

Seminars in Immunology

Pub Date : 2025-03-27 DOI: 10.1016/j.smim.2025.101945

Monika Bradl , Qian Yu , Yoshiki Takai

Ever since the discovery of pathogenic aquaporin 4-specific antibodies in the serum of patients with neuromyelitis optica spectrum disorders current knowledge about clinical observations and diagnosis, and about the underlying pathology and resulting therapies have been put forward in excellent reviews and primary publications. However, in order to further develop novel strategies for the treatment of this disease, there is an urgent need to understand the immunological processes associated with the formation of the pathogenic antibodies, and with aberrant immune responses observed in affected patients. In this review, we will highlight and evaluate important studies on these processes.

自从在视神经脊髓炎患者的血清中发现致病性水通道蛋白4特异性抗体以来，目前关于临床观察和诊断，以及潜在病理和由此产生的治疗的知识已经在优秀的综述和主要出版物中提出。然而，为了进一步开发治疗这种疾病的新策略，迫切需要了解与致病性抗体形成相关的免疫过程，以及在患者中观察到的异常免疫反应。在这篇综述中，我们将重点介绍和评价这些过程的重要研究。

引用次数: 0

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Insights into pathogenesis and biomarkers of prognosis 髓鞘少突胶质细胞糖蛋白抗体相关疾病（MOGAD）：发病机制和预后生物标志物的见解

IF 7.4 2区医学 Q1 IMMUNOLOGY

Seminars in Immunology

Pub Date : 2025-03-14 DOI: 10.1016/j.smim.2025.101944

Jane Andersen , Fabienne Brilot

MOG antibody-associated disease (MOGAD), an inflammatory demyelinating pathology, is typically associated with the clinical phenotypes acute disseminated encephalomyelitis (ADEM), optic neuritis (ON), or transverse myelitis (TM). The mainstay of diagnosis is detection of antibodies targeting oligodendrocyte-expressed MOG (MOG-IgG). MOG-IgG-mediated demyelination occurs via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), enhanced cognate T-cell CNS infiltration and activation, and oligodendrocyte cytoskeleton disruption, but the exact role of the immune system in MOGAD is still poorly understood. The disease course is either monophasic or relapsing, with relapsing course affecting approximately two-thirds of individuals. Neurological disability accumulates with relapse and may manifest as visual, motor, sensory, and cognitive deficits. Thus, accurate disease course prediction is of paramount importance. Prognostic biomarkers, implemented at a global scale, have the potential to guide timely therapeutic decisions to limit relapse-associated disability accrual while simultaneously avoiding unnecessary immunosuppression in monophasic individuals. This review explores recent insights in the understanding of MOGAD pathogenesis as well as advances in prognostic biomarkers of relapsing course and disease activity.

MOG抗体相关疾病（MOGAD）是一种炎症性脱髓鞘病理，通常与临床表型急性播散性脑脊髓炎（ADEM）、视神经炎（ON）或横断性脊髓炎（TM）相关。诊断的主要方法是检测针对少突胶质细胞表达的MOG （MOG- igg）的抗体。mog - igg介导的脱髓鞘通过补体依赖性细胞毒性（CDC）、抗体依赖性细胞毒性（ADCC）、同源t细胞CNS浸润和激活增强以及少突胶质细胞骨架破坏发生，但免疫系统在MOGAD中的确切作用仍然知之甚少。病程为单相或复发，复发病程影响约三分之二的个体。神经功能障碍随着复发而积累，表现为视觉、运动、感觉和认知缺陷。因此，准确的病程预测至关重要。在全球范围内实施的预后生物标志物有可能指导及时的治疗决策，以限制复发相关残疾的累积，同时避免单相患者不必要的免疫抑制。本文综述了最近对MOGAD发病机制的认识以及复发过程和疾病活动性预后生物标志物的进展。

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引用次数: 0

Differential immune responses behind different celiac disease manifestations 不同乳糜泻表现背后的免疫反应差异

IF 7.4 2区医学 Q1 IMMUNOLOGY

Seminars in Immunology

Pub Date : 2025-03-13 DOI: 10.1016/j.smim.2025.101941

Esko Kemppainen, Olga Albó, Helka Kaunisto, Emilia Siukola, Katri Lindfors

In celiac disease (CeD), dietary gluten serves as the driver for a comparatively well characterized small bowel mucosal immune response that generally results in small bowel mucosal villous atrophy and crypt hyperplasia along with a disease-specific transglutaminase 2 (TG2) targeting autoantibody response. Individuals with positive TG2 autoantibodies but normal small intestinal mucosal morphology are regarded at increased risk of developing CeD and represent patients with potential CeD. The removal of gluten from the diet leads to disappearance of the autoantibodies and normalization of the mucosal architecture in most cases. However, refractory CeD patients deviate from this dogma as they present with abnormal T cell compartment, persistent symptoms and villous atrophy despite a strict gluten-free diet. The heterogeneity of CeD presentation is further diversified by varying symptomatology. Gastrointestinal symptoms are the most canonical signs of CeD, and they include for instance diarrhea, vomiting, constipation and abdominal pain. Yet, a great portion of the patients manifest the disease at extraintestinal sites such as skin, musculoskeletal system or neuronal tissues. Beyond the involvement of various transglutaminase autoantibodies, the detailed immune mechanisms contributing to the development of these manifestations remains elusive, though. This review highlights the current understanding of the immunological differences in various manifestations of CeD. As the immunological basis of the different CeD phenotypes is at present insufficiently understood, more research on the subject is warranted before such data could be maximally applied to clinical practice.

在乳糜泻（CeD）中，膳食麸质是小肠黏膜免疫反应的驱动因素，这种免疫反应通常导致小肠黏膜绒毛萎缩和隐窝增生，同时伴有疾病特异性的转谷氨酰胺酶2 （TG2）靶向自身抗体反应。TG2自身抗体阳性但小肠黏膜形态正常的个体被认为是发生CeD的风险增加，并代表潜在的CeD患者。在大多数情况下，从饮食中去除麸质会导致自身抗体的消失和粘膜结构的正常化。然而，难治性CeD患者偏离了这一教条，因为他们表现出异常的T细胞室，持续的症状和绒毛萎缩，尽管严格的无麸质饮食。由于不同的症状，CeD表现的异质性进一步多样化。胃肠道症状是CeD最典型的症状，包括腹泻、呕吐、便秘和腹痛。然而，很大一部分患者的疾病表现在肠外部位，如皮肤、肌肉骨骼系统或神经组织。除了各种转谷氨酰胺酶自身抗体的参与之外，促成这些表现发展的详细免疫机制仍然难以捉摸。本文综述了目前对CeD各种表现的免疫学差异的认识。由于目前对不同CeD表型的免疫学基础了解不足，在这些数据能够最大限度地应用于临床实践之前，需要对该主题进行更多的研究。

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引用次数: 0

Neuroimmune interactions between itch neurons and skin microbes 瘙痒神经元和皮肤微生物之间的神经免疫相互作用

IF 7.4 2区医学 Q1 IMMUNOLOGY

Seminars in Immunology

Pub Date : 2025-03-08 DOI: 10.1016/j.smim.2025.101933

Sharan Kumar Balaji , Waris Muhammad Khuwaja , Md Liakat Hossain , Luchiano Giovanni Benjamin Fernando, Xintong Dong

Itch is an unpleasant sensation that is encoded by specific sensory neurons called pruriceptors. Itch is associated with almost all skin diseases. Recent studies revealed that many itchy skin diseases are associated with microbiome dysbiosis. Pathogenic microbes secrete proteases and toxins to invade skin cells. Some microbial products can directly activate sensory neurons, while others activate the mammalian immune system and indirectly cause itch. In this review, we summarize the current knowledge on microbe-immune-neuron crosstalks and discuss their relevance in itchy skin diseases.

痒是一种不愉快的感觉，是由一种叫做瘙痒感受器的特殊感觉神经元编码的。几乎所有的皮肤病都与瘙痒有关。最近的研究表明，许多皮肤瘙痒性疾病与微生物群失调有关。病原微生物分泌蛋白酶和毒素侵入皮肤细胞。一些微生物产物可以直接激活感觉神经元，而另一些则可以激活哺乳动物的免疫系统，间接引起瘙痒。本文综述了微生物-免疫-神经元串扰的最新研究进展，并讨论了它们在皮肤瘙痒性疾病中的相关性。

引用次数: 0