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Background: Bats harbor various viruses without severe symptoms and act as their natural reservoirs. The tolerance of bats against viral infections is assumed to originate from the uniqueness of their immune system. However, how immune responses vary between primates and bats remains unclear. Here, we characterized differences in the immune responses by peripheral blood mononuclear cells to various pathogenic stimuli between primates (humans, chimpanzees, and macaques) and bats (Egyptian fruit bats) using single-cell RNA sequencing.
Results: We show that the induction patterns of key cytosolic DNA/RNA sensors and antiviral genes differed between primates and bats. A novel subset of monocytes induced by pathogenic stimuli specifically in bats was identified. Furthermore, bats robustly respond to DNA virus infection even though major DNA sensors are dampened in bats.
Conclusions: Overall, our data suggest that immune responses are substantially different between primates and bats, presumably underlying the difference in viral pathogenicity among the mammalian species tested.
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http://dx.doi.org/10.1093/gigascience/giad086 | DOI Listing |
Curr Opin Lipidol
August 2025
Cardiometabolic Immunity Laboratory, Department of Physiology, Monash Biomedicine Discovery Institute (BDI) and Victorian Heart Institute (VHI), Monash University, Melbourne, Victoria, Australia.
Purpose Of Review: This review explores the evolving understanding of efferocytosis - the clearance of dead or dying cells by phagocytes - in the context of atherosclerosis. It highlights recent discovers in cell death modalities, impaired clearance mechanisms and emerging therapeutic strategies aimed at restoring efferocytosis to stabilize plaques and resolve inflammation.
Recent Findings: Recent studies have expanded the scope of efferocytosis beyond apoptotic cells to include other pro-inflammatory cell death modes, including pyroptosis, necroptosis and ferroptosis, revealing context-dependent clearance efficiency and immunological outcomes.
Macrophage Migration Inhibitory Factor (MIF) is a pleiotropic cytokine that acts as a central regulator of inflammation and immune responses across diverse organ systems. Functioning upstream in immune activation cascades, MIF influences macrophage polarization, T and B cell differentiation, and cytokine expression through CD74, CXCR2/4/7, and downstream signaling via NF-κB, ERK1/2, and PI3K/AKT pathways. This review provides a comprehensive analysis of MIF's mechanistic functions under both physiological and pathological conditions, highlighting its dual role as a protective mediator during acute stress and as a pro-inflammatory amplifier in chronic disease.
View Article and Find Full Text PDFClin Exp Immunol
September 2025
Rheumatology Department, Université Paris-Saclay, Institut National de la Santé et de la Recherche Médicale (INSERM) UMR1184, Hôpital Bicêtre, Assistance Publique-Hôpitaux de Paris (APHP), CEA , FHU CARE, Le Kremlin Bicêtre, France.
Introduction: Immunosenescence remodels immune functions and was first described with aging. It is present in 25% of cancer patients but has also been described in patients with Immune-mediated inflammatory diseases (IMIDs). This study aims at quantifying cells exhibiting a phenotype of senescence in CD4+ (T4sen) and CD8+ (T8sen) T cells, analyzing its potential drivers and the effect of anti-TNF treatment in a prospective cohort of patients with rheumatoid arthritis (RA), spondyloarthritis (SpA) and Sjögren disease (SjD).
View Article and Find Full Text PDFCarcinogenesis
September 2025
Department of Medicine, Gastroenterology and Hepatology Division, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611-3010, USA.
Esophageal cancer is a major cause of cancer-related death, often preceded with chronic inflammation and injuries. The NFκB/IKKβ pathway plays a central role in inflammation, yet its role in early esophageal carcinogenesis remains unclear. This study investigated the role of epithelial IKKβ in early esophageal carcinogenesis.
View Article and Find Full Text PDFBMB Rep
September 2025
Department of Microbiology and Immunology, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea; Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea; Institute for Immunology and Immunological Diseases, Yonsei Uni
B cell tolerance is critical for preventing autoimmunity, yet the mechanisms by which B cells discriminate self from non-self antigens remain incompletely understood. While early findings emphasize the role of classical antigen-mediated BCR signaling strength by varying antigen formats, emerging evidence highlights the importance of mechanical cues during antigen recognition. This review explores how mechanosensitive ion channels, particularly Piezo1, contribute to B cell activation and tolerance by integrating physical forces at the immune synapse.
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