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Scooped by
Gilbert C FAURE
May 29, 2015 8:21 AM
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The TOP 10% information you need!
The scoops deal with published (classical or OPEN) and grey literature (blogs, websites, social networks, press releases) allowing rapid access to recently published relevant information May 29, 2015 you were 26796 visitors, viewing this topic 34.5K times., 4900 scoops June 2020 : >7.3K scoops, >94.5K visitors, #121K views August 2022: >7.8K scoops, >96,2K visitors, >133,7K views December 2023: >8K scoops, >97,7K vis, >171,3K views
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Scooped by
Gilbert C FAURE
June 6, 2:22 AM
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Phagocytosis is the process by which myeloid phagocytes bind to and internalize potentially dangerous microorganisms1. During phagocytosis, innate immune receptors and associated signalling proteins are localized to the maturing phagosome compartment, forming an immune information processing hub brimming with microorganism-sensing features2–8. Here we developed proximity labelling of phagosomal contents (PhagoPL) to identify proteins localizing to phagosomes containing model yeast and bacteria. By comparing the protein composition of phagosomes containing evolutionarily and biochemically distinct microorganisms, we unexpectedly identified programmed death-ligand 1 (PD-L1) as a protein that specifically enriches in phagosomes containing yeast. We found that PD-L1 directly binds to yeast upon processing in phagosomes. By surface display library screening, we identified the ribosomal protein Rpl20b as a fungal protein ligand for PD-L1. Using an auxin-inducible depletion system, we found that detection of Rpl20b by macrophages cross-regulates production of distinct cytokines including interleukin-10 (IL-10) induced by the activation of other innate immune receptors. Thus, this study establishes PhagoPL as a useful approach to quantifying the collection of proteins enriched in phagosomes during host–microorganism interactions, exemplified by identifying PD-L1 as a receptor that binds to fungi. Proximity labelling of phagosomal contents is used to identify proteins that localize to phagosomes in host–microorganism interactions.
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Scooped by
Gilbert C FAURE
May 28, 11:18 AM
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The majority of cancer patients receive radiotherapy. Wang et al. review preclinical and clinical data related to the importance of immune responses to rad
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Scooped by
Gilbert C FAURE
May 13, 4:39 AM
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Scooped by
Gilbert C FAURE
May 7, 11:37 AM
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Leukocyte migration is a fundamental component of innate and adaptive immune responses as it governs the recruitment and localization of these motile cells, which is crucial for immune cell priming, effector functions, memory responses and immune regulation. This complex cellular trafficking system is controlled to a large extent via highly regulated production of secreted chemokines and the restricted expression of their membrane-tethered G-protein-coupled receptors. The activity of chemokines and their receptors is also regulated by a subfamily of molecules known as atypical chemokine receptors (ACKRs), which are chemokine receptor-like molecules that do not couple to the classical signalling pathways that promote cell migration in response to chemokine ligation. There has been a great deal of progress in understanding the biology of these receptors and their functions in the immune system in the past decade. Here, we describe the contribution of the various ACKRs to innate and adaptive immune responses, focussing specifically on recent progress. This includes recent findings that have defined the role for ACKRs in sculpting extracellular chemokine gradients, findings that broaden the spectrum of chemokine ligands recognized by these receptors, candidate new additions to ACKR family, and our increasing understanding of the role of these receptors in shaping the migration of innate and adaptive immune cells. This Review from Comerford and McColl discusses recent advances that have been made in understanding the biology of the atypical chemokine receptor (ACKR) family. The authors explain how these receptors interact with their ligands to shape immune responses and also highlight potential new additions to the ACKR family.
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Scooped by
Gilbert C FAURE
May 5, 12:57 PM
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This work reveals that human effector CD8 T cells not only mediate cytotoxicity but also promote tissue remodeling. The remodeling potential was demonstrat
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Scooped by
Gilbert C FAURE
May 2, 5:10 AM
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Scooped by
Gilbert C FAURE
April 30, 6:36 AM
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Scooped by
Gilbert C FAURE
April 29, 4:21 AM
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29 avril 2024 | 2h00 - 4h30 CET | En ligne
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Scooped by
Gilbert C FAURE
April 26, 5:13 AM
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Scooped by
Gilbert C FAURE
April 18, 5:26 AM
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Scooped by
Gilbert C FAURE
April 15, 8:03 AM
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Scooped by
Gilbert C FAURE
April 7, 9:46 AM
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Scooped by
Gilbert C FAURE
June 10, 8:54 AM
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Influenza virus infection is initiated by the attachment of the viral haemagglutinin (HA) protein to sialic acid receptors on the host cell surface. Most virus particles enter cells through clathrin-mediated endocytosis (CME). However, it is unclear how viral binding signals are transmitted through the plasma membrane triggering CME. Here we found that metabotropic glutamate receptor subtype 2 (mGluR2) and potassium calcium-activated channel subfamily M alpha 1 (KCa1.1) are involved in the initiation and completion of CME of influenza virus using an siRNA screen approach. Influenza virus HA directly interacted with mGluR2 and used it as an endocytic receptor to initiate CME. mGluR2 interacted and activated KCa1.1, leading to polymerization of F-actin, maturation of clathrin-coated pits and completion of the CME of influenza virus. Importantly, mGluR2-knockout mice were significantly more resistant to different influenza subtypes than the wild type. Therefore, blocking HA and mGluR2 interaction could be a promising host-directed antiviral strategy. Influenza virus uses metabotropic glutamate receptor 2 (mGluR2) as an endocytic receptor to enter cells through clathrin-mediated endocytosis.
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Scooped by
Gilbert C FAURE
June 4, 4:29 AM
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Immune memory — comprising T cells, B cells and plasma cells and their secreted antibodies — is crucial for human survival. It enables the rapid and effective clearance of a pathogen after re-exposure, to minimize damage to the host. When antigen-experienced, memory T cells become activated, they proliferate and produce effector molecules at faster rates and in greater magnitudes than antigen-inexperienced, naive cells. Similarly, memory B cells become activated and differentiate into antibody-secreting cells more rapidly than naive B cells, and they undergo processes that increase their affinity for antigen. The ability of T cells and B cells to form memory cells after antigen exposure is the rationale behind vaccination. Understanding immune memory not only is crucial for the design of more-efficacious vaccines but also has important implications for immunotherapies in infectious disease and cancer. This ‘guide to’ article provides an overview of the current understanding of the phenotype, function, location, and pathways for the generation, maintenance and protective capacity of memory T cells and memory B cells. This Review provides a guide to the memory cells of the adaptive immune system, comprising memory T cells, memory B cells and plasma cells; it covers their formation, function, heterogeneity, localization, regulation and maintenance, and the crucial technological advances that allowed their discovery.
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Scooped by
Gilbert C FAURE
May 27, 7:08 AM
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Summary. Basophils are the rarest leukocytes, but they have essential roles in protection against helminths, allergic disorders, autoimmune diseases, and s
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Scooped by
Gilbert C FAURE
May 10, 3:47 AM
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CD4 T helper cells use the SNARE protein SYNTAXIN-11 to promote B cell differentiation, germinal center formation, and class switching by facilitating CD40
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Scooped by
Gilbert C FAURE
May 5, 1:19 PM
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The authors show that early Th2 cell differentiation is driven via prolonged T–DC macro-clustering in lymph nodes and occurs in a skin site-specific manner
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Scooped by
Gilbert C FAURE
May 3, 2:39 AM
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A Blueprint for #Tumor-Infiltrating #Bcells across Human #Cancers | Breaking OPEN ACCESS Study Online Now at Science Magazine + Accompanying OPEN ACCESS…
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Scooped by
Gilbert C FAURE
April 30, 10:29 AM
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Today we celebrate the incredible advancements in immunology that help protect us from disease and pave the way for healthier futures.
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Scooped by
Gilbert C FAURE
April 29, 4:26 AM
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Have you ever wondered why, during the COVID-19 pandemic, the elderly were at greater risk for severe disease, often resulting in hospitalisations, ICU admissions and even death? And why did most children not show any symptoms, despite being infected with the same virus? Then, you’ll find this year’s theme for the International Day of Immunology particularly intriguing: ‘Immunity through the ages’.
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Scooped by
Gilbert C FAURE
April 29, 4:20 AM
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Day of Immunology Celebrate your amazing immune system on the 29 April by attending events around Australia and New Zealand. Established in 2005 by the European Federation of Immunological Societies (EFIS), the success of Day of Immunology led to it being celebrated worldwide since 2007.
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Scooped by
Gilbert C FAURE
April 26, 4:25 AM
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Editor’s summary In response to infection, a small protein called interferon-γ (IFN-γ) is synthesized and released by several types of cells belonging to the immune system. IFN-γ acts on both immune and nonimmune cells to provide protection against bacteria, parasites, and fungi. Casanova et al. review how advances in IFN-γ research and the study of conditions resulting from IFN-γ deficiencies have, together, improved understanding of host protection and specific contributions provided by IFN-γ. Moreover, the authors evaluate the prospects of using IFN-γ as a therapeutic agent for infectious disease. —Sarah H. Ross
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Scooped by
Gilbert C FAURE
April 15, 8:09 AM
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Scooped by
Gilbert C FAURE
April 8, 10:59 AM
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Abstract. Transplanted organs carry donor immune cells into the recipient, the majority of which are tissue-resident macrophages (TRMs). The role they play
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Scooped by
Gilbert C FAURE
March 24, 9:28 AM
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Plus de 30 ans après la dernière épidémie importante au Québec, la rougeole fait à nouveau les manchettes. Des chercheurs tentent de comprendre comment le virus réussit à anéantir l’immunité contre d’autres maladies.
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Keystone, not much snow?