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| http://dx.doi.org/10.1016/j.htct.2022.11.007 | DOI Listing |
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Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38.
Front Immunol
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Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet and University of Oslo, Oslo, Norway.
Introduction: CD38, a regulator of intracellular calcium signalling, is highly expressed in immune cells. Mice lacking CD38 are very susceptible to acute bacterial infections, implicating CD38 in innate immune responses. The effects of CD38 inhibition on NLRP3 inflammasome activation in human primary monocytes and monocyte-derived macrophages have not been investigated.
View Article and Find Full Text PDFHumanized anti-CD11d monoclonal antibodies suitable for basic research and therapeutic applications.
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Department of Microbiology & Immunology and Robarts Research Institute, University of Western Ontario, London, Ontario N6A 5B7, Canada.
Background: Immunomodulatory agents targeting the CD11d/CD18 integrin are in development for the treatment of several pathophysiologies including neurotrauma, sepsis, and atherosclerosis. Murine anti-human CD11d therapeutic antibodies have successfully improved neurological and behavioral recovery in rodent neurotrauma models. Here, we present the progression of CD11d-targeted agents with the development of humanized anti-CD11d monoclonal antibodies.
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Department of Anatomy, Faculty of Medicine, Masaryk University, Brno, Czechia.
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View Article and Find Full Text PDFReplicating Dynamic Immune Responses at Single-Cell Resolution within a Microfluidic Human Skin Equivalent.
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Centre for Cell Biology and Cutaneous Research, Blizard Institute, Queen Mary University of London, 4 Newark Street, London, E1 2AT, UK.
To enable in vitro investigation of human skin immunology, this study develops a microfluidic human skin equivalent (HSE) that supports the delivery of circulating immune cells via a vascular microchannel embedded within the dermis of a full-thickness construct. Within this platform, activation of keratinocyte inflammation promotes monocyte migration out of the vascular channel and into the dermal and epidermal compartments. Single-cell transcriptomic analysis reveals dynamic and cell-specific patterns of gene expression that are characteristic of acute activation and resolution of an inflammatory immune response, and the gene signatures of the monocyte-derived cells closely matches the differentiation trajectory of the monocytes into mature dermal macrophages.
View Article and Find Full Text PDFInjured Myocardium-Targeted Theranostic Nanoplatform for Multi-Dimensional Immune-Inflammation Regulation in Acute Myocardial Infarction.
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Department of Radiology, Nanjing Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, 305 East Zhongshan Road, Nanjing, 210002, China.
Pyroptosis is a key mode of programmed cell death during the early stages following acute myocardial infarction (AMI), driving immune-inflammatory responses. Cardiac resident macrophages (CRMs) are the primary mediators of cardiac immunity, and they serve a dual role through their shaping of both myocardial injury and post-AMI myocardial repair. To appropriately regulate AMI-associated inflammation, HM4oRL is herein designed, an innovative bifunctional therapeutic nanoplatform capable of inhibiting cardiomyocyte pyroptosis while reprogramming inflammatory signaling.
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