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Airway macrophage glycolysis controls lung homeostasis and responses to aeroallergen. 气道巨噬细胞糖酵解控制着肺的稳态和对空气过敏原的反应。
IF 7.9 2区 医学 Q1 IMMUNOLOGY Pub Date : 2024-10-18 DOI: 10.1016/j.mucimm.2024.10.002
Gesa J Albers, Christina Michalaki, Patricia P Ogger, Amy F Lloyd, Benjamin Causton, Simone A Walker, Anna Caldwell, John M Halket, Linda V Sinclair, Sarah H Forde, Cormac McCarthy, Timothy S C Hinks, Clare M Lloyd, Adam J Byrne

The lungs represent a dynamic microenvironment where airway macrophages (AMs) are the major lung-resident macrophages. AMs dictate the balance between tissue homeostasis and immune activation and thus have contradictory functions by maintaining tolerance and tissue homeostasis, as well as initiating strong inflammatory responses. Emerging evidence has highlighted the connection between macrophage function and cellular metabolism. However, the functional importance of these processes in tissue-resident specialized macrophage populations such as those found in the airways, remain poorly elucidated. Here, we reveal that glycolysis is a fundamental pathway in AMs which regulates both lung homeostasis and responses to inhaled allergen. Using macrophage specific targeting in vivo, and multi-omics approaches, we determined that glycolytic activity in AMs is necessary to restrain type 2 (T2) immunity during homeostasis. Exposure to a range of common aeroallergens, including house dust mite (HDM), drove AM-glycolysis and furthermore, AM-specific inhibition of glycolysis altered inflammation in the airways and HDM-driven airway metabolic adaptations in vivo. Additionally, allergen sensitised asthmatics had profound metabolic changes in the airways, compared to non-sensitised asthmatic controls. Finally, we found that allergen driven AM-glycolysis in mice was TLR2 dependent. Thus, our findings demonstrate a direct relationship between glycolysis in AMs, AM-mediated homeostatic processes, and T2 immune responses in the lungs. These data suggest that glycolysis is essential for the plasticity of AMs. Depending on the immunological context, AM-glycolysis is required to exert homeostatic activity but once activated by allergen, AM-glycolysis influences inflammatory responses. Thus, precise modulation of glycolytic activity in AMs is essential for preserving lung homeostasis and regulating airway inflammation.

肺是一个动态的微环境,气道巨噬细胞(AMs)是驻肺的主要巨噬细胞。巨噬细胞决定着组织稳态和免疫激活之间的平衡,因此具有相互矛盾的功能,既能维持耐受性和组织稳态,又能引发强烈的炎症反应。新的证据强调了巨噬细胞功能与细胞新陈代谢之间的联系。然而,这些过程在组织驻留的特化巨噬细胞群(如在呼吸道中发现的巨噬细胞群)中的功能重要性仍未得到充分阐明。在这里,我们揭示了糖酵解是巨噬细胞的一个基本途径,它同时调节着肺的稳态和对吸入过敏原的反应。利用体内巨噬细胞特异性靶向和多组学方法,我们确定了AMs中的糖酵解活性是在体内平衡过程中抑制2型(T2)免疫所必需的。暴露于包括屋尘螨(HDM)在内的一系列常见空气过敏原会促进AM糖酵解,此外,AM特异性糖酵解抑制会改变气道炎症和HDM驱动的体内气道代谢适应。此外,与未致敏的哮喘对照组相比,过敏原致敏的哮喘患者的气道代谢发生了深刻变化。最后,我们发现过敏原驱动的小鼠 AM 糖酵解作用依赖于 TLR2。因此,我们的研究结果表明,AM 中的糖酵解、AM 介导的体内平衡过程和肺部的 T2 免疫反应之间存在直接关系。这些数据表明,糖酵解对 AM 的可塑性至关重要。根据不同的免疫环境,AM-糖酵解需要发挥稳态活性,但一旦被过敏原激活,AM-糖酵解就会影响炎症反应。因此,精确调节AMs中的糖酵解活性对于保持肺稳态和调节气道炎症至关重要。
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引用次数: 0
RelB and C/EBPα critically regulate the development of Peyer's patch mononuclear phagocytes. RelB和C/EBPα对Peyer's patch单核吞噬细胞的发育具有关键性调控作用。
IF 7.9 2区 医学 Q1 IMMUNOLOGY Pub Date : 2024-10-14 DOI: 10.1016/j.mucimm.2024.10.005
Takashi Kanaya, Toshi Jinnohara, Sayuri Sakakibara, Naoko Tachibana, Takaharu Sasaki, Tamotsu Kato, Marc Riemann, Jianshi Jin, Katsuyuki Shiroguchi, Eiryo Kawakami, Hiroshi Ohno

To establish protection against harmful foreign antigens, the small intestine harbors guardian sites called Peyer's patches (PPs). PPs take up antigens through microfold (M) cells and transfer them to the sub-epithelial dome (SED), which contains a high density of mononuclear phagocytes (MPs), for T cell-priming. Accumulating evidence indicates that SED-MPs have unique functions other than T cell-priming to facilitate mucosal immune responses; however, the crucial factors regulating the functions of SED-MPs have not been determined. Here we performed transcriptome analysis, and identified the gene signatures of SED-MPs. Further data interpretation with transcription factor (TF) enrichment analysis estimated TFs responsible for the functions of SED-MPs. Among them, we found that RelB and C/EBPα were preferentially activated in SED-MPs. RelB-deficiency silenced the expression of IL-22BP and S100A4 by SED-MPs. On the other hand, C/EBPα-deficiency decreased the expression of lysozyme by SED-MPs, resulting the increased invasion of orally administered pathogenic bacteria into PPs and mesenteric lymph nodes. Our findings thus demonstrate that RelB and C/EBPα are essential to regulate the functions of SED-MPs.

为了抵御有害的外来抗原,小肠内有一个名为 "佩尔斑块"(Peyer's patches,PPs)的守护点。PPs通过微褶(M)细胞吸收抗原,并将其转移到上皮下穹隆(SED),后者含有高密度的单核吞噬细胞(MPs),用于T细胞吸附。越来越多的证据表明,SED-MPs 除了促进粘膜免疫反应的 T 细胞唤醒功能外,还具有其他独特的功能;然而,调控 SED-MPs 功能的关键因素尚未确定。在此,我们进行了转录组分析,并确定了 SED-MPs 的基因特征。通过转录因子(TF)富集分析对数据进行进一步解读,推测出负责 SED-MPs 功能的 TFs。其中,我们发现RelB和C/EBPα在SED-MPs中优先被激活。RelB缺陷抑制了SED-MPs对IL-22BP和S100A4的表达。另一方面,C/EBPα缺陷降低了SED-MPs表达溶菌酶的能力,导致口服致病菌侵入PPs和肠系膜淋巴结的能力增强。因此,我们的研究结果表明,RelB和C/EBPα对调控SED-MPs的功能至关重要。
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引用次数: 0
TRIM29 controls enteric RNA virus-induced intestinal inflammation by targeting NLRP6 and NLRP9b signaling pathways. TRIM29 通过靶向 NLRP6 和 NLRP9b 信号通路控制肠道 RNA 病毒诱导的肠道炎症。
IF 7.9 2区 医学 Q1 IMMUNOLOGY Pub Date : 2024-10-11 DOI: 10.1016/j.mucimm.2024.10.004
Junying Wang, Ling Wang, Wenting Lu, Naser Farhataziz, Anastasia Gonzalez, Junji Xing, Zhiqiang Zhang

Infections by enteric virus and intestinal inflammation are recognized as a leading cause of deadly gastroenteritis, and NLRP6 and NLRP9b signaling control these infection and inflammation. However, the regulatory mechanisms of the NLRP6 and NLRP9b signaling in enteric viral infection remain unexplored. In this study, we found that the E3 ligase TRIM29 suppressed type III interferon (IFN-λ) and interleukin-18 (IL-18) production by intestinal epithelial cells (IECs) when exposed to polyinosinic:polycytidylic acid (poly I:C) and enteric RNA viruses. Knockout of TRIM29 in IECs was efficient to restrict intestinal inflammation triggered by the enteric RNA viruses, rotavirus in suckling mice, and the encephalomyocarditis virus (EMCV) in adults. This attenuation in inflammation was attributed to the increased production of IFN-λ and IL-18 in the IECs and more recruitment of intraepithelial protective Ly6A+CCR9+CD4+ T cells in small intestines from TRIM29-deficient mice. Mechanistically, TRIM29 promoted K48-linked ubiquitination, leading to the degradation of NLRP6 and NLRP9b, resulting in decreased IFN-λ and IL-18 secretion by IECs. Our findings reveal that enteric viruses utilize TRIM29 to inhibit IFN-λ and inflammasome activation in IECs, thereby facilitating viral-induced intestinal inflammation. This indicates that targeting TRIM29 could offer a promising therapeutic strategy for alleviating gut diseases.

肠道病毒感染和肠道炎症被认为是致命性肠胃炎的主要原因,而 NLRP6 和 NLRP9b 信号传导控制着这些感染和炎症。然而,NLRP6 和 NLRP9b 信号在肠道病毒感染中的调控机制仍有待探索。在这项研究中,我们发现当肠道上皮细胞(IECs)暴露于多聚肌苷酸:多聚胞苷酸(poly I:C)和肠道RNA病毒时,E3连接酶TRIM29会抑制III型干扰素(IFN-λ)和白细胞介素-18(IL-18)的产生。在 IECs 中敲除 TRIM29 能有效限制肠道 RNA 病毒、乳鼠轮状病毒和成人脑心肌炎病毒(EMCV)引发的肠道炎症。炎症的减轻归因于 IECs 中 IFN-λ 和 IL-18 的产生增加,以及 TRIM29 缺失小鼠小肠中上皮内保护性 Ly6A+CCR9+CD4+ T 细胞的招募增加。从机理上讲,TRIM29促进了与K48相连的泛素化,导致NLRP6和NLRP9b降解,从而使IECs分泌的IFN-λ和IL-18减少。我们的研究结果表明,肠道病毒利用 TRIM29 抑制 IFN-λ 和 IECs 中炎性体的激活,从而促进病毒诱导的肠道炎症。这表明,靶向 TRIM29 可为缓解肠道疾病提供一种前景广阔的治疗策略。
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引用次数: 0
A reappraisal of IL-9 in inflammation and cancer. 重新评估 IL-9 在炎症和癌症中的作用。
IF 7.9 2区 医学 Q1 IMMUNOLOGY Pub Date : 2024-10-09 DOI: 10.1016/j.mucimm.2024.10.003
Fabian Bick, Christophe Blanchetot, Bart N Lambrecht, Martijn J Schuijs

While much is known about the functional effects of type 2 cytokines interleukin (IL)-4, IL-5 and IL-13 in homeostasis and disease, we still poorly understand the functions of IL-9. Chronic inflammation seen in allergic diseases, autoimmunity and cancer is however frequently accompanied by overproduction of this elusive type 2 cytokine. Initially identified as a T cell and mast cell growth factor, and later as the hallmark cytokine defining TH9 cells, we now know that IL-9 is produced by multiple innate and adaptive immune cells. Recent evidence suggests that IL-9 controls discrete aspects of the allergic cascade, cellular responses of immune and stromal cells, cancer progression, tolerance and immune escape. Despite functioning as a pleiotropic cytokine in mucosal environments, like the lungs, the direct and indirect cellular targets of IL-9 are still not well characterized. Here, we discuss IL-9's cellular senders and receivers, focusing on asthma and cancer. Moreover, we review current research directions and the outlook of targeted therapy centered around the biology of IL-9.

尽管人们对白细胞介素(IL)-4、IL-5 和 IL-13 等 2 型细胞因子在体内平衡和疾病中的功能作用了解甚多,但对 IL-9 的功能却知之甚少。然而,过敏性疾病、自身免疫性疾病和癌症中的慢性炎症常常伴随着这种难以捉摸的 2 型细胞因子的过度分泌。最初,IL-9 被认为是一种 T 细胞和肥大细胞生长因子,后来又被认为是界定 TH9 细胞的标志性细胞因子,现在我们知道 IL-9 由多种先天性和适应性免疫细胞产生。最近的证据表明,IL-9 控制着过敏级联、免疫细胞和基质细胞的细胞反应、癌症进展、耐受性和免疫逃逸等不同方面。尽管IL-9在肺部等粘膜环境中发挥着多种细胞因子的作用,但其直接和间接细胞靶点的特征仍不十分明确。在此,我们将以哮喘和癌症为重点,讨论 IL-9 的细胞发送者和接收者。此外,我们还回顾了当前的研究方向以及以 IL-9 的生物学特性为中心的靶向治疗的前景。
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引用次数: 0
Sensory neuroimmune interactions at the barrier. 屏障上的感官神经免疫相互作用
IF 7.9 2区 医学 Q1 IMMUNOLOGY Pub Date : 2024-10-05 DOI: 10.1016/j.mucimm.2024.10.001
Zhen Wang, Keaton Song, Brian S Kim, John Manion

Epithelial barriers such as the skin, lung, and gut, in addition to having unique physiologic functions, are designed to preserve tissue homeostasis upon challenge with a variety of allergens, irritants, or pathogens. Both the innate and adaptive immune systems play a critical role in responding to epithelial cues triggered by environmental stimuli. However, the mechanisms by which organs sense and coordinate complex epithelial, stromal, and immune responses have remained a mystery. Our increasing understanding of the anatomic and functional characteristics of the sensory nervous system is greatly advancing a new field of peripheral neuroimmunology and subsequently changing our understanding of mucosal immunology. Herein, we detail how sensory biology is informing mucosal neuroimmunology, even beyond neuroimmune interactions seen within the central and autonomic nervous systems.

皮肤、肺部和肠道等上皮屏障除了具有独特的生理功能外,还能在受到各种过敏原、刺激物或病原体的挑战时保持组织平衡。先天性免疫系统和适应性免疫系统在对环境刺激引发的上皮线索做出反应方面都起着至关重要的作用。然而,器官感知和协调复杂的上皮、基质和免疫反应的机制一直是个谜。我们对感觉神经系统的解剖和功能特征的理解不断加深,这极大地推动了外周神经免疫学这一新领域的发展,并随之改变了我们对粘膜免疫学的理解。在此,我们将详细介绍感觉生物学如何为粘膜神经免疫学提供信息,甚至超越中枢神经系统和自主神经系统内的神经免疫相互作用。
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引用次数: 0
Bite-sized immunology; damage and microbes educating immunity at the gingiva 咬合免疫学;损害和微生物教育牙龈免疫。
IF 7.9 2区 医学 Q1 IMMUNOLOGY Pub Date : 2024-10-01 DOI: 10.1016/j.mucimm.2024.07.004
Immune cells residing at the gingiva experience diverse and unique signals, tailoring their functions to enable them to appropriately respond to immunological challenges and maintain tissue integrity. The gingiva, defined as the mucosal barrier that surrounds and supports the teeth, is the only barrier site completely transected by a hard structure, the tooth. The tissue is damaged in early life during tooth eruption and chronically throughout life by the process of mastication. This occurs alongside challenges typical of barrier sites, including exposure to invading pathogens, the local commensal microbial community and environmental antigens. This review will focus on the immune network safeguarding gingival integrity, which is far less understood than that resident at other barrier sites. A detailed understanding of the gingiva-resident immune network is vital as it is the site of the inflammatory disease periodontitis, the most common chronic inflammatory condition in humans which has well-known detrimental systemic effects. Furthering our understanding of how the immune populations within the gingiva develop, are tailored in health, and how this is dysregulated in disease would further the development of effective therapies for periodontitis.
驻留在牙龈的免疫细胞会经历各种独特的信号,从而调整其功能,使其能够对免疫挑战做出适当的反应,并保持组织的完整性。牙龈被定义为环绕和支撑牙齿的粘膜屏障,是唯一一个被坚硬结构--牙齿--完全横切的屏障部位。牙龈组织在生命早期的牙齿萌出过程中受到损伤,并在整个生命过程中因咀嚼而长期受到损伤。这与屏障部位所面临的典型挑战同时发生,包括暴露于入侵病原体、当地共生微生物群落和环境抗原。本综述将重点讨论保护牙龈完整性的免疫网络,人们对该网络的了解远远少于对其他屏障部位的了解。详细了解牙龈驻留的免疫网络至关重要,因为牙龈是炎症性疾病牙周炎的发病部位,而牙周炎是人类最常见的慢性炎症性疾病,具有众所周知的有害全身影响。进一步了解牙龈内的免疫群体是如何发展的、在健康状态下是如何调整的,以及在疾病状态下是如何失调的,将有助于开发治疗牙周炎的有效疗法。
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引用次数: 0
Long-term alterations in lung epithelial cells after EL-RSV infection exacerbate allergic responses through IL-1β-induced pathways EL-RSV感染后肺上皮细胞的长期改变通过IL-1β诱导途径加剧过敏反应运行标题:EL-RSV 和长期改变。
IF 7.9 2区 医学 Q1 IMMUNOLOGY Pub Date : 2024-10-01 DOI: 10.1016/j.mucimm.2024.07.007
Early-life (EL) respiratory infections increase pulmonary disease risk, especially EL-Respiratory Syncytial Virus (EL-RSV) infections linked to asthma. Mechanisms underlying asthma predisposition remain unknown. In this study, we examined the long-term effects on the lung after four weeks post EL-RSV infection. We identified alterations in the lung epithelial cell, with a rise in the percentage of alveolar type 2 epithelial cells (AT2) and a decreased percentage of cells in the AT1 and AT2-AT1 subclusters, as well as upregulation of Bmp2 and Krt8 genes that are associated with AT2-AT1 trans-differentiation, suggesting potential defects in lung repair processes. We identified persistent upregulation of asthma-associated genes, including Il33. EL-RSV-infected mice allergen-challenged exhibited exacerbated allergic response, with significant upregulation of Il33 in the lung and AT2 cells. Similar long-term effects were observed in mice exposed to EL-IL-1β. Notably, treatment with IL-1ra during acute EL-RSV infection mitigated the long-term alveolar alterations and the allergen-exacerbated response. Finally, epigenetic modifications in the promoter of the Il33 gene were detected in AT2 cells harvested from EL-RSV and EL-IL1β groups, suggesting that long-term alteration in the epithelium after RSV infection is dependent on the IL-1β pathway. This study provides insight into the molecular mechanisms of asthma predisposition after RSV infection.
生命早期(EL)呼吸道感染会增加肺部疾病风险,尤其是与哮喘有关的EL-呼吸道合胞病毒(EL-RSV)感染。哮喘易感性的机制仍不清楚。在本研究中,我们研究了 EL-RSV 感染四周后对肺部的长期影响。我们发现肺上皮细胞发生了改变,肺泡2型上皮细胞(AT2)的比例上升,AT1和AT2-AT1亚群细胞的比例下降,与AT2-AT1跨分化相关的Bmp2和Krt8基因上调,这表明肺修复过程存在潜在缺陷。我们发现了哮喘相关基因(包括 Il33)的持续上调。EL-RSV 感染的小鼠在过敏原挑战下表现出加剧的过敏反应,肺部和 AT2 细胞中的 Il33 显著上调。在暴露于 EL-IL-1β 的小鼠中也观察到了类似的长期效应。值得注意的是,在急性EL-RSV感染期间用IL-1ra治疗可减轻肺泡的长期改变和过敏原加重的反应。最后,在 EL-RSV 组和 EL-IL1β 组收获的 AT2 细胞中检测到了 Il33 基因启动子的表观遗传修饰,这表明 RSV 感染后上皮细胞的长期改变依赖于 IL-1β 途径。这项研究有助于深入了解 RSV 感染后哮喘易感性的分子机制。
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引用次数: 0
Local antigen encounter promotes generation of tissue-resident memory T cells in the large intestine 局部抗原相遇可促进大肠中组织驻留记忆 T 细胞的生成。
IF 7.9 2区 医学 Q1 IMMUNOLOGY Pub Date : 2024-10-01 DOI: 10.1016/j.mucimm.2024.05.005
Upon infection, CD8+ T cells that have been primed in the draining lymph nodes migrate to the invaded tissue, where they receive cues prompting their differentiation into tissue-resident memory cells (Trm), which display niche-specific transcriptional features. Despite the importance of these cells, our understanding of their molecular landscape and the signals that dictate their development remains limited, particularly in specific anatomical niches such as the large intestine (LI). Here, we report that LI Trm-generated following oral infection exhibits a distinct transcriptional profile compared to Trm in other tissues. Notably, we observe that local cues play a crucial role in the preferential establishment of LI Trm, favoring precursors that migrate to the tissue early during infection. Our investigations identify cognate antigen recognition as a major driver of Trm differentiation at this anatomical site. Local antigen presentation not only promotes the proliferation of effector cells and memory precursors but also facilitates the acquisition of transcriptional features characteristic of gut Trm. Thus, antigen recognition in the LI favors the establishment of Trm by impacting T cell expansion and gene expression.
感染后,在引流淋巴结中被激活的 CD8+ T 细胞会迁移到受侵袭的组织,在那里它们会接收到促使它们分化为组织驻留记忆细胞(Trm)的信号,这些细胞会显示出龛位特异性转录特征。尽管这些细胞非常重要,但我们对其分子图谱和决定其发育的信号的了解仍然有限,尤其是在大肠(LI)等特定解剖龛位中。在这里,我们报告了口腔感染后产生的大肠Trm与其他组织中的Trm相比表现出不同的转录特征。值得注意的是,我们观察到局部线索在 LI Trm 的优先建立中起着至关重要的作用,有利于感染期间早期迁移到该组织的前体。我们的研究发现,同源抗原识别是这一解剖部位Trm分化的主要驱动力。局部抗原呈递不仅能促进效应细胞和记忆前体的增殖,还能促进获得肠道Trm特有的转录特征。因此,LI 中的抗原识别会影响 T 细胞的扩增和基因表达,从而有利于 Trm 的建立。
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引用次数: 0
Activated eosinophils in early life impair lung development and promote long-term lung damage 生命早期活化的嗜酸性粒细胞会损害肺部发育并促进长期肺损伤。
IF 7.9 2区 医学 Q1 IMMUNOLOGY Pub Date : 2024-10-01 DOI: 10.1016/j.mucimm.2024.06.003
Exaggeration of type 2 immune responses promotes lung inflammation and altered lung development; however, eosinophils, despite expansion in the postnatal lung, have not been specifically assessed in the context of neonatal lung disease. Furthermore, early life factors including prematurity and respiratory infection predispose infants to chronic obstructive pulmonary disease later in life. To assess eosinophils in the developing lung and how they may contribute to chronic lung disease, we generated mice harboring eosinophil-specific deletion of the negative regulatory enzyme SH2 domain-containing inositol 5′ phosphatase-1. This increased the activity and number of pulmonary eosinophils in the developing lung, which was associated with impaired lung development, expansion of activated alveolar macrophages (AMφ), multinucleated giant cell formation, enlargement of airspaces, and fibrosis. Despite regression of eosinophils following completion of lung development, AMφ-dominated inflammation persisted, alongside lung damage. Bone marrow chimera studies showed that SH2 domain-containing inositol 5′ phosphatase-1-deficient eosinophils were not sufficient to drive inflammatory lung disease in adult steady-state mice but once inflammation and damage were present, it could not be resolved. Depletion of eosinophils during alveolarization alleviated pulmonary inflammation and lung pathology, demonstrating an eosinophil-intrinsic effect. These results show that the presence of activated eosinophils during alveolarization aggravates AMφs and promotes sustained inflammation and long-lasting lung pathology.
2型免疫反应的加剧会促进肺部炎症和肺部发育的改变;然而,尽管嗜酸性粒细胞在出生后肺部扩大,但尚未对新生儿肺部疾病进行专门评估。此外,包括早产和呼吸道感染在内的生命早期因素使婴儿日后易患慢性阻塞性肺病。为了评估发育中肺部的嗜酸性粒细胞及其对慢性肺病的影响,我们培育了嗜酸性粒细胞特异性缺失负调控酶 SHIP-1 的小鼠。这增加了发育中肺部嗜酸性粒细胞的活性和数量,导致肺发育受损、活化肺泡巨噬细胞(AMφ)扩张、多核巨细胞形成、气孔扩大和纤维化。尽管嗜酸性粒细胞在肺发育完成后有所减少,但以 AMφ 为主的炎症仍持续存在,同时还伴有肺损伤。骨髓嵌合体研究表明,SHIP-1缺陷的嗜酸性粒细胞不足以驱动成年稳态小鼠的肺部炎症,但炎症和损伤一旦出现,就无法解决。在肺泡化过程中消耗嗜酸性粒细胞可缓解肺部炎症和肺部病理变化,这证明了嗜酸性粒细胞的内在效应。这些结果表明,肺泡化过程中活化的嗜酸性粒细胞会加重 AMφs,并促进持续的炎症和长期的肺部病变。
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引用次数: 0
Dietary protein modulates intestinal dendritic cells to establish mucosal homeostasis 膳食蛋白质调节肠道树突状细胞,建立粘膜稳态。
IF 7.9 2区 医学 Q1 IMMUNOLOGY Pub Date : 2024-10-01 DOI: 10.1016/j.mucimm.2024.06.006
Dietary proteins are taken up by intestinal dendritic cells (DCs), cleaved into peptides, loaded to major histocompatibility complexes, and presented to T cells to generate an immune response. Amino acid (AA)-diets do not have the same effects because AAs cannot bind to major histocompatibility complex to activate T cells. Here, we show that impairment in regulatory T cell generation and loss of tolerance in mice fed a diet lacking whole protein is associated with major transcriptional changes in intestinal DCs including downregulation of genes related to DC maturation, activation and decreased gene expression of immune checkpoint molecules. Moreover, the AA-diet had a profound effect on microbiome composition, including an increase in Akkermansia muciniphilia and Oscillibacter and a decrease in Lactococcus lactis and Bifidobacterium. Although microbiome transfer experiments showed that AA-driven microbiome modulates intestinal DC gene expression, most of the unique transcriptional change in DC was linked to the absence of whole protein in the diet. Our findings highlight the importance of dietary proteins for intestinal DC function and mucosal tolerance.
膳食蛋白质会被肠道树突状细胞(DC)吸收,裂解成肽,装载到主要组织相容性配体(MHC)上,并呈现给 T 细胞以产生免疫反应。氨基酸(AA)饮食没有同样的效果,因为AA不能与MHC结合以激活T细胞。在这里,我们发现,以缺乏全蛋白的饮食喂养的小鼠的 Treg 细胞生成障碍和耐受性丧失与肠道 DC 的主要转录变化有关,包括 DC 成熟、活化和迁移相关基因的下调以及免疫检查点分子基因表达的减少。此外,AA饮食对微生物组的组成也有深远影响,包括Akkermansia muciniphilia和Oscillibacter的增加以及乳酸乳球菌和双歧杆菌的减少。虽然微生物组转移实验表明 AA 驱动的微生物组会调节肠道直肠基因表达,但直肠中大多数独特的转录变化都与膳食中缺乏全蛋白质有关。我们的研究结果凸显了膳食蛋白质对肠道直流电功能和粘膜耐受性的重要性。
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引用次数: 0
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Mucosal Immunology
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