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Novel insights into the dynamic function of PRC2 in innate immunity. 对 PRC2 在先天性免疫中动态功能的新认识。
IF 13.1 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-11-27 DOI: 10.1016/j.it.2024.10.003
Rosalie W M Kempkes, Rab K Prinjha, Menno P J de Winther, Annette E Neele

The polycomb repressive complex 2 (PRC2) is an established therapeutic target in cancer. PRC2 catalyzes methylation of histone H3 at lysine 27 (H3K27me3) and is known for maintaining eukaryote cell identity. Recent discoveries show that modulation of PRC2 not only impacts cell differentiation and tumor growth but also has immunomodulatory properties. Here, we integrate multiple immunological fields to understand PRC2 and its subunits in epigenetic canonical regulation and non-canonical mechanisms within innate immunity. We discuss how PRC2 regulates hematopoietic stem cell proliferation, myeloid cell differentiation, and shapes innate immune responses. The PRC2 catalytic domain EZH2 is upregulated in various human inflammatory diseases and its deletion or inhibition in experimental mouse models can reduce disease severity, emphasizing its importance in regulating inflammation.

多聚核抑制复合体 2(PRC2)是癌症的一个公认治疗靶点。PRC2 催化组蛋白 H3 在赖氨酸 27 处的甲基化(H3K27me3),以维持真核细胞特性而闻名。最近的发现表明,对 PRC2 的调节不仅会影响细胞分化和肿瘤生长,还具有免疫调节特性。在这里,我们整合了多个免疫学领域,以了解 PRC2 及其亚基在先天性免疫中的表观遗传规范调控和非规范机制。我们将讨论 PRC2 如何调控造血干细胞增殖、髓系细胞分化以及影响先天性免疫反应。PRC2催化域EZH2在各种人类炎症疾病中上调,在实验小鼠模型中删除或抑制EZH2可减轻疾病的严重程度,这强调了它在调节炎症中的重要性。
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引用次数: 0
Unanticipated specificity in effector-triggered immunity. 效应器触发免疫中意想不到的特异性。
IF 13.1 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-11-15 DOI: 10.1016/j.it.2024.10.008
Alejandra Zárate-Potes, Hinrich Schulenburg, Katja Dierking

Effector-triggered immunity (ETI) enables hosts to react to pathogens by monitoring few key cellular processes. ETI responses are assumed to be similar toward related pathogen effectors. However, recent evidence from the invertebrate model Caenorhabditis elegans and pore-forming toxins indicates a much more complex and specific ETI than previously anticipated.

效应触发免疫(ETI)使宿主能够通过监测一些关键的细胞过程对病原体做出反应。一般认为,ETI 对相关病原体效应物的反应是相似的。然而,最近来自无脊椎动物模型秀丽隐杆线虫和孔形成毒素的证据表明,ETI 比以前预期的要复杂得多,也具体得多。
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引用次数: 0
The immune-endocrine interplay in sex differential responses to viral infection and COVID-19. 免疫-内分泌在对病毒感染和 COVID-19 的性别差异反应中的相互作用。
IF 13.1 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-11-18 DOI: 10.1016/j.it.2024.10.004
Valentino D'Onofrio, Rafick Pierre Sékaly

Men are at higher risk for developing severe COVID-19 than women, while women are at higher risk for developing post-acute sequelae of COVID-19 (PASC). This highlights the impact of sex differences on immune responses and clinical outcomes of acute COVID-19 or PASC. A dynamic immune-endocrine interface plays an important role in the development of effective immune responses impacting the control of viral infections. In this opinion article we discuss mechanisms underlying the transcriptional and epigenetic regulation of immune responses by sex hormones during viral infections. We propose that disruption of this delicate immune-endocrine interplay can result in worsened outcomes of viral disease. We also posit that insights into these immune mechanisms can propel the development of novel immunomodulatory interventions that leverage immune-endocrine pathways to treat viral infections.

与女性相比,男性罹患严重 COVID-19 的风险更高,而女性罹患 COVID-19 急性后遗症(PASC)的风险更高。这凸显了性别差异对急性 COVID-19 或 PASC 的免疫反应和临床结果的影响。在影响病毒感染控制的有效免疫反应的发展过程中,动态的免疫-内分泌界面发挥着重要作用。在这篇观点性文章中,我们讨论了病毒感染期间性激素对免疫反应的转录和表观遗传调控机制。我们认为,破坏这种微妙的免疫-内分泌相互作用会导致病毒性疾病恶化。我们还认为,对这些免疫机制的了解可以推动新型免疫调节干预措施的开发,从而利用免疫-内分泌途径治疗病毒感染。
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引用次数: 0
Neuroimmune interactions in the olfactory epithelium: maintaining a sensory organ at an immune barrier interface. 嗅觉上皮细胞的神经免疫相互作用:在免疫屏障界面上维持一个感觉器官。
IF 13.1 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-11-15 DOI: 10.1016/j.it.2024.10.005
Mohammed N Ullah, Nicholas R Rowan, Andrew P Lane

While primarily a sensory organ, the mammalian olfactory epithelium (OE) also plays a critical role as an immune barrier. Mechanisms governing interactions between the immune system and this specialized chemosensory tissue are gaining interest, in part sparked by the COVID-19 pandemic. Regulated inflammation is intrinsic to normal mucosal healing and homeostasis, but prolonged OE inflammation is associated with persistent loss of smell, belying the intertwining of local mucosal immunology and olfactory function. Evidence supports bidirectional communication between OE cells and the immune system in health and disease. Recent investigations suggest that neuro-immune cross-talk modulates olfactory stem cell behavior and neuronal regeneration dynamics, prioritizing the epithelial-like non-neuronal framework with immune barrier function at the expense of the neurosensory organ in chronic inflammation.

哺乳动物的嗅上皮(OE)虽然主要是一个感觉器官,但同时也扮演着免疫屏障的重要角色。部分由于 COVID-19 大流行而引发的免疫系统与这种特化的化学感觉组织之间的相互作用机制正受到越来越多的关注。调节性炎症是粘膜正常愈合和平衡的内在因素,但长期的OE炎症与持续的嗅觉丧失有关,这表明局部粘膜免疫与嗅觉功能是相互交织的。有证据表明,在健康和疾病状态下,嗅觉器官细胞与免疫系统之间存在双向交流。最近的研究表明,神经-免疫交叉对话可调节嗅觉干细胞的行为和神经元再生动态,在慢性炎症中优先考虑具有免疫屏障功能的上皮样非神经元框架,而牺牲神经感觉器官。
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引用次数: 0
SARS-CoV-2 reprograms murine alveolar macrophages to dampen flu. SARS-CoV-2 使小鼠肺泡巨噬细胞重编程,从而抑制流感。
IF 13.1 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-11-22 DOI: 10.1016/j.it.2024.11.002
Alexandra Tabachnikova, Akiko Iwasaki

Innate immune cells that are epigenetically reprogrammed by infection can modify host responses to subsequent infections. Lercher et al. have identified epigenetic reprogramming of murine airway-resident macrophages following recovery from SARS-CoV-2 infection, conferring protection from pathology and lethality following secondary influenza A virus (IAV) challenge without reducing viral titers.

先天免疫细胞因感染而发生表观遗传重编程,可改变宿主对后续感染的反应。Lercher 等人发现,小鼠气道驻留巨噬细胞在从 SARS-CoV-2 感染中恢复后进行了表观遗传学重编程,从而在甲型流感病毒(IAV)的二次挑战中免于病理变化和致死,而病毒滴度却没有降低。
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引用次数: 0
Cytosolic delivery of innate immune agonists. 先天性免疫激动剂的胞浆输送。
IF 13.1 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-11-19 DOI: 10.1016/j.it.2024.10.007
Ravi Bharadwaj, Swati Jaiswal, Neal Silverman

Solute carrier proteins (SLCs) are pivotal for maintaining cellular homeostasis by transporting small molecules across cellular membranes. Recent discoveries have uncovered their involvement in modulating innate immunity, particularly within the cytosol. We review emerging evidence that links SLC transporters to cytosolic innate immune recognition and highlight their role in regulating inflammation. We explore how SLC transporters influence the activation of endosomal Toll-like receptors, cytosolic NODs, and STING sensors. Understanding the contribution of SLCs to innate immune recognition provides insight into their fundamental biological functions and opens new avenues to develop possible therapeutic interventions for autoimmune and inflammatory diseases. This review aims to discuss current knowledge and identify key gaps in this rapidly evolving field.

溶质运载蛋白(SLCs)通过跨细胞膜运输小分子来维持细胞的平衡。最近的发现揭示了它们参与调节先天性免疫,尤其是在细胞膜内。我们回顾了将 SLC 转运体与细胞膜先天性免疫识别联系起来的新证据,并强调了它们在调节炎症中的作用。我们探讨了 SLC 转运体如何影响内膜 Toll 样受体、细胞膜 NOD 和 STING 传感器的激活。了解 SLC 对先天性免疫识别的贡献有助于深入了解它们的基本生物功能,并为开发治疗自身免疫性和炎症性疾病的干预措施开辟了新途径。本综述旨在讨论当前的知识,并找出这一快速发展领域的关键差距。
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引用次数: 0
Weapon of choice: viruses share cross-kingdom tools. 首选武器:病毒共享跨领域工具。
IF 13.1 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-11-21 DOI: 10.1016/j.it.2024.11.006
C J E Metcalf, B Koskella

Following on from the discovery that innate immune pathways are shared widely across the tree of life comes another surprise: Hobbs et al. show that viruses targeting animals and bacteria also use highly conserved tools to fight back. Why such mechanisms remain seemingly unchanged despite the rapid coevolution among hosts and pathogens is now a key open question for the field.

继发现先天性免疫途径在生命之树上广泛共享之后,又一个惊喜出现了:霍布斯等人的研究表明,针对动物和细菌的病毒也使用高度保守的工具进行反击。尽管宿主和病原体之间发生了快速的共同进化,但为什么这种机制似乎保持不变,这是目前该领域的一个关键性开放问题。
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引用次数: 0
Approaches for studying neuroimmune interactions in Alzheimer's disease. 研究阿尔茨海默病神经免疫相互作用的方法。
IF 13.1 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-11-12 DOI: 10.1016/j.it.2024.10.002
Chih-Chung 'Jerry' Lin, Yuyao Tian, Rudolph E Tanzi, Mehdi Jorfi

Peripheral immune cells play an important role in the pathology of Alzheimer's disease (AD), impacting processes such as amyloid and tau protein aggregation, glial activation, neuronal integrity, and cognitive decline. Here, we examine cutting-edge strategies - encompassing animal and cellular models - used to investigate the roles of peripheral immune cells in AD. Approaches such as antibody-mediated depletion, genetic ablation, and bone marrow chimeras in mouse models have been instrumental in uncovering T, B, and innate immune cell disease-modifying functions. However, challenges such as specificity, off-target effects, and differences between human and mouse immune systems underscore the need for more human-relevant models. Emerging multicellular models replicating critical aspects of human brain tissue and neuroimmune interactions increasingly offer fresh insights into the role of immune cells in AD pathogenesis. Refining these methodologies can deepen our understanding of immune cell contributions to AD and support the development of novel immune-related therapeutic interventions.

外周免疫细胞在阿尔茨海默病(AD)的病理过程中发挥着重要作用,影响着淀粉样蛋白和 tau 蛋白聚集、神经胶质细胞活化、神经元完整性和认知能力下降等过程。在此,我们将探讨用于研究外周免疫细胞在阿尔茨海默病中的作用的前沿策略--包括动物和细胞模型。小鼠模型中的抗体介导耗竭、基因消融和骨髓嵌合体等方法有助于发现T、B和先天性免疫细胞的疾病调节功能。然而,特异性、脱靶效应以及人类和小鼠免疫系统之间的差异等挑战突出表明,我们需要更多与人类相关的模型。新出现的多细胞模型复制了人类脑组织和神经免疫相互作用的关键方面,越来越多地提供了免疫细胞在艾滋病发病机制中作用的新见解。完善这些方法可以加深我们对免疫细胞在艾滋病中的作用的了解,并支持开发新型免疫相关治疗干预措施。
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引用次数: 0
The peptide selectivity model: Interpreting NK cell KIR-HLA-I binding interactions and their associations to human diseases. 多肽选择性模型:解读 NK 细胞 KIR-HLA-I 结合相互作用及其与人类疾病的关联。
IF 13.1 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-11-21 DOI: 10.1016/j.it.2024.10.006
Malcolm J W Sim, Eric O Long

Combinations of the highly polymorphic KIR and HLA-I genes are associated with numerous human diseases. Interpreting these associations requires a molecular understanding of the multiple killer-cell immunoglobulin-like receptor (KIR)-human leukocyte antigen-1 (HLA-I) receptor-ligand interactions on natural killer (NK) cells and identifying the salient features that underlie disease risk. We hypothesize that a critical discriminating factor in KIR-HLA-I interactions is the selective detection of HLA-I-bound peptides by KIRs. We propose a 'peptide selectivity model', where high-avidity KIR-HLA-I interactions reflect low selectivity for peptides conferring consistent NK cell inhibition across different tissue immunopeptidomes. Conversely, lower-avidity interactions (including those with activating KIRs) are more dependent on HLA-I-bound peptide sequence, requiring an appreciation of how HLA-I immunopeptidomes influence KIR binding and regulate NK cell function. Relevant to understanding NK cell function and pathology, we interpret known KIR-HLA-I combinations and their associations with certain human diseases in the context of this 'peptide selectivity model'.

高度多态的 KIR 和 HLA-I 基因组合与许多人类疾病相关。解读这些关联需要从分子角度了解自然杀伤(NK)细胞上的多种杀伤细胞免疫球蛋白样受体(KIR)-人类白细胞抗原-1(HLA-I)受体-配体的相互作用,并确定疾病风险的显著特征。我们假设,KIR-HLA-I 相互作用的一个关键鉴别因素是 KIR 对 HLA-I 结合肽的选择性检测。我们提出了一个 "肽选择性模型",即高活性的 KIR-HLA-I 相互作用反映了对肽的低选择性,从而在不同组织免疫肽组中产生一致的 NK 细胞抑制作用。相反,低度相互作用(包括与激活型 KIR 的相互作用)则更依赖于 HLA-I 结合的肽序列,因此需要了解 HLA-I 免疫肽组如何影响 KIR 结合并调节 NK 细胞功能。为了了解 NK 细胞的功能和病理学,我们将在这种 "肽选择性模型 "的背景下解释已知的 KIR-HLA-I 组合及其与某些人类疾病的关联。
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引用次数: 0
Please don't go: retinoic acid 'retains' tissue-specific memory. 请不要走:维甲酸 "保留 "组织特异性记忆。
IF 13.1 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-11-20 DOI: 10.1016/j.it.2024.11.005
Michal A Stanczak, Erika L Pearce

Tissue-resident memory (TRM) T cells not only control infection and cancer, but also contribute to inflammatory disease. In a recent study, Obers et al. demonstrate that retinoic acid (RA) and TGF-β direct TRM residency in mice, with RA uniquely retaining cells in the intestine by limiting migration. This discovery highlights the potential for harnessing local residency cues to enhance tissue-specific TRM responses.

组织驻留记忆(TRM)T细胞不仅能控制感染和癌症,还能引发炎症性疾病。在最近的一项研究中,Obers 等人证明了视黄酸(RA)和 TGF-β 能引导小鼠体内 TRM 的驻留,其中视黄酸通过限制迁移独特地将细胞保留在肠道中。这一发现凸显了利用局部驻留线索增强组织特异性 TRM 反应的潜力。
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引用次数: 0
期刊
Trends in Immunology
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