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Systematic identification of cell state-specific transcription factors in T cells
IF 67.7 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-12-09 DOI: 10.1038/s41577-024-01118-1
Didem Ağaç Çobanoğlu
A preprint by Chung et al. presents a framework for the use of transcriptomic and epigenomic data to identify novel transcription factors driving CD8+ T cell states.
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引用次数: 0
Neuroinflammation in Alzheimer disease
IF 67.7 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-12-09 DOI: 10.1038/s41577-024-01104-7
Michael T. Heneka, Wiesje M. van der Flier, Frank Jessen, Jeroen Hoozemanns, Dietmar Rudolf Thal, Delphine Boche, Frederic Brosseron, Charlotte Teunissen, Henrik Zetterberg, Andreas H. Jacobs, Paul Edison, Alfredo Ramirez, Carlos Cruchaga, Jean-Charles Lambert, Agustin Ruiz Laza, Jose Vicente Sanchez-Mut, Andre Fischer, Sergio Castro-Gomez, Thor D. Stein, Luca Kleineidam, Michael Wagner, Jonas J. Neher, Colm Cunningham, Sim K. Singhrao, Marco Prinz, Christopher K. Glass, Johannes C. M. Schlachetzki, Oleg Butovsky, Kilian Kleemann, Philip L. De Jaeger, Hannah Scheiblich, Guy C. Brown, Gary Landreth, Miguel Moutinho, Jaime Grutzendler, Diego Gomez-Nicola, Róisín M. McManus, Katrin Andreasson, Christina Ising, Deniz Karabag, Darren J. Baker, Shane A. Liddelow, Alexei Verkhratsky, Malu Tansey, Alon Monsonego, Ludwig Aigner, Guillaume Dorothée, Klaus-Armin Nave, Mikael Simons, Gabriela Constantin, Neta Rosenzweig, Alberto Pascual, Gabor C. Petzold, Jonathan Kipnis, Carmen Venegas, Marco Colonna, Jochen Walter, Andrea J. Tenner, M. Kerry O’Banion, Joern R. Steinert, Douglas L. Feinstein, Magdalena Sastre, Kiran Bhaskar, Soyon Hong, Dorothy P. Schafer, Todd Golde, Richard M. Ransohoff, David Morgan, John Breitner, Renzo Mancuso, Sean-Patrick Riechers
Increasing evidence points to a pivotal role of immune processes in the pathogenesis of Alzheimer disease, which is the most prevalent neurodegenerative and dementia-causing disease of our time. Multiple lines of information provided by experimental, epidemiological, neuropathological and genetic studies suggest a pathological role for innate and adaptive immune activation in this disease. Here, we review the cell types and pathological mechanisms involved in disease development as well as the influence of genetics and lifestyle factors. Given the decade-long preclinical stage of Alzheimer disease, these mechanisms and their interactions are driving forces behind the spread and progression of the disease. The identification of treatment opportunities will require a precise understanding of the cells and mechanisms involved as well as a clear definition of their temporal and topographical nature. We will also discuss new therapeutic strategies for targeting neuroinflammation, which are now entering the clinic and showing promise for patients. This Review provides an in-depth examination of how inflammation contributes to neurodegeneration in Alzheimer disease. The authors explore the impact of extrinsic factors, such as brain trauma, diet and infections, and host-intrinsic factors, such as the activity of microglial cells and other immune, vascular and neuronal cell populations, on disease development. They also highlight emerging drugs that target this inflammatory component for therapy of Alzheimer disease.
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引用次数: 0
Author Correction: Inflammasome components as new therapeutic targets in inflammatory disease
IF 67.7 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-12-05 DOI: 10.1038/s41577-024-01123-4
Rebecca C. Coll, Kate Schroder
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引用次数: 0
Publisher Correction: Inflammasome components as new therapeutic targets in inflammatory disease
IF 67.7 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-12-05 DOI: 10.1038/s41577-024-01122-5
Rebecca C. Coll, Kate Schroder
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引用次数: 0
Guardians of immune privilege
IF 67.7 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-12-03 DOI: 10.1038/s41577-024-01121-6
Yvonne Bordon
Endogenous self-peptides derived from CNS antigens are presented on MHC class II molecules at the borders of the CNS and expand suppressive populations of CD4+ T cells.
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引用次数: 0
Sialylated IgG restrains lung inflammation
IF 67.7 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-11-29 DOI: 10.1038/s41577-024-01120-7
Lucy Bird
Sialylated IgG protects against severe influenza by inducing the transcriptional repressor REST, which dampens the inflammatory response and preserves lung tissue function.
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引用次数: 0
Mitochondria in monocyte-derived cells promote tissue damage in multiple sclerosis 单核细胞衍生细胞中的线粒体促进了多发性硬化症的组织损伤
IF 67.7 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-11-26 DOI: 10.1038/s41577-024-01116-3
Zi Yan Chen, Arthur Mortha
A preprint by Villar-Vesga et al. shows that monocyte-derived cells in the central nervous system produce mitochondrial reactive oxygen species to promote neuroinflammation.
Villar-Vesga 等人的预印本显示,中枢神经系统中的单核细胞衍生细胞会产生线粒体活性氧,从而促进神经炎症。
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引用次数: 0
Redefining PD1 as a guardian of stem-like T cells 将 PD1 重新定义为干样 T 细胞的守护者
IF 67.7 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-11-25 DOI: 10.1038/s41577-024-01117-2
Matthew Jackson, Eileen E. Parkes
A preprint by Hor et al. shows that PD1 signalling regulates the maintenance of a high-affinity, stem-like T cell subset in tumour-draining lymph nodes.
Hor等人的预印本显示,PD1信号调节着肿瘤引流淋巴结中高亲和性干样T细胞亚群的维持。
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引用次数: 0
Integrating natural commensals and pathogens into preclinical mouse models 将天然共生菌和病原体纳入临床前小鼠模型
IF 67.7 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-11-19 DOI: 10.1038/s41577-024-01108-3
Barbara Rehermann, Andrea L. Graham, David Masopust, Sara E. Hamilton
Fundamental discoveries in many aspects of mammalian physiology have been made using laboratory mice as research models. These studies have been facilitated by the genetic tractability and inbreeding of such mice, the large set of immunological reagents that are available, and the establishment of environmentally controlled, high-throughput facilities. Such facilities typically include barriers to keep the mouse colonies free of pathogens and the frequent re-derivation of the mice severely limits their commensal flora. Because humans have co-evolved with microorganisms and are exposed to a variety of pathogens, a growing community of researchers posits that preclinical disease research can be improved by studying mice in the context of the microbiota and pathogens that they would encounter in the natural world. Here, we provide a perspective of how these different approaches can be combined and integrated to improve existing mouse models to enhance our understanding of disease mechanisms and develop new therapies for humans. We also propose that the term ‘mice with natural microbiota’ is more appropriate for describing these models than existing terms such as ‘dirty mice’. There is emerging evidence that mice with a history of microbial exposures can better model the human immune system than laboratory mice maintained in pathogen-free conditions. In this Perspective, Rehermann and colleagues summarize different approaches that have been used to incorporate microbiota and pathogen exposures into laboratory mouse models. They suggest that the term ‘mice with natural microbiota’ should be used instead of ‘dirty mice’ to describe these systems in the future.
以实验小鼠为研究模型,已经在哺乳动物生理学的许多方面取得了重大发现。这些研究得益于小鼠在遗传学上的可操作性和近亲繁殖、大量可用的免疫试剂以及环境可控的高通量设施的建立。这些设施通常包括一些屏障,以保持小鼠群落中没有病原体,而且小鼠的频繁再繁殖严重限制了它们的共生菌群。由于人类与微生物共同进化并接触各种病原体,越来越多的研究人员认为,在小鼠在自然界中会遇到的微生物群和病原体的背景下研究小鼠,可以改进临床前疾病研究。在此,我们将从一个角度来探讨如何将这些不同的方法结合起来并加以整合,以改进现有的小鼠模型,从而提高我们对疾病机理的认识,并为人类开发出新的疗法。我们还提出,与 "脏小鼠 "等现有术语相比,"天然微生物群小鼠 "更适合描述这些模型。
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引用次数: 0
Innate lymphoid cell control of neuronal synapse development 先天性淋巴细胞控制神经元突触的发育
IF 67.7 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-11-19 DOI: 10.1038/s41577-024-01113-6
Katherine Whalley
ILC2s promote inhibitory synapse formation in the postnatal mouse brain through the production of IL-13.
ILC2 通过产生 IL-13 促进出生后小鼠大脑抑制性突触的形成。
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引用次数: 0
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Nature Reviews Immunology
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