The ability of the innate and adaptive immune systems to communicate with each other is central to protective immune responses and maintenance of host health. Myeloid cells of the innate immune system are able to sense microbial ligands, perturbations in cellular homeostasis, and virulence factors, thereby allowing them to relay distinct pathogen-specific information to naïve T cells in the form of pathogen-derived peptides and a unique cytokine milieu. Once primed, effector T helper cells produce lineage-defining cytokines to help combat the original pathogen, and a subset of these cells persist as memory or effector-memory populations. These memory T cells then play a dual role in host protection by not only responding rapidly to reinfection, but by also directly instructing myeloid cells to express licensing cytokines. This means there is a bi-directional flow of information first from the innate to the adaptive immune system, and then from the adaptive back to innate immune system. Here, we focus on how signals, first from pathogens and then from primed effector and memory T cells, are integrated by myeloid cells and its consequences for protective immunity or systemic inflammation.
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http://dx.doi.org/10.1016/j.coi.2021.07.013 | DOI Listing |
Front Immunol
January 2025
Institute for Experimental Immunology and Imaging, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Post-stroke early activation of neutrophils contributes to intensive neuroinflammation and worsens disease outcomes. Other pre-existing patient conditions can modify the extent of their activation during disease, especially hypercholesterolemia. However, whether and how increased circulating cholesterol amounts can change neutrophil activation responses very early after stroke has not been studied.
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January 2025
Key Laboratory of Chinese Medicine Rheumatology of Zhejiang Province, Research Institute of Chinese Medical Clinical Foundation and Immunology, College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.
Background: SLE and ME/CFS both present significant fatigue and share immune dysregulation. The mechanisms underlying fatigue in these disorders remain unclear, and there are no standardized treatments. This study aims to explore shared mechanisms and predict potential therapeutic drugs for fatigue in SLE and ME/CFS.
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January 2025
Institut National de la Santé et de la Recherche Médicale (INSERM), Unité Mixte de Recherche U1236, Université Rennes, Etablissement Français du Sang Bretagne, LabEx IGO, Rennes, France.
Introduction: Myeloid cells trafficking from the periphery to the central nervous system are key players in multiple sclerosis (MS) through antigen presentation, cytokine secretion and repair processes.
Methods: Combination of mass cytometry on blood cells from 60 MS patients at diagnosis and 29 healthy controls, along with single cell RNA sequencing on paired blood and cerebrospinal fluid (CSF) samples from 5 MS patients were used for myeloid cells detailing.
Results: Myeloid compartment study demonstrated an enrichment of a peculiar classical monocyte population in 22% of MS patients at the time of diagnosis.
Front Immunol
January 2025
Instituto de Investigaciones Bioquímicas de La Plata "Prof. Dr. Rodolfo R. Brenner", (INIBIOLP), Universidad Nacional de La Plata (UNLP) - Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), La Plata, Argentina.
Introduction: Gastropod hemocyanins are potent immunostimulants in mammals, a trait associated with their large molecular size and unusual glycosylation patterns. While the hemocyanin from the marine snail keyhole limpet (KLH), has been widely studied and successfully employed as a carrier/adjuvant in several immunological applications, as well as a non-specific immunostimulant for bladder cancer treatment, few other gastropod hemocyanins have been biochemically and immunologically characterized. In this work, we investigated the immunogenic properties of the hemocyanin from (PcH), an invasive south American freshwater snail.
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January 2025
Department of Rheumatology, The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui, China.
Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation and progressive joint destruction. Neutrophil extracellular traps (NETs), a microreticular structure formed after neutrophil death, have recently been implicated in RA pathogenesis and pathological mechanisms. However, the underlying molecular mechanisms and key genes involved in NET formation in RA remain largely unknown.
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