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Type I Interferon Targets Alveolar Macrophages to Promote Bacterial Pneumonia after Viral Infection.
Am J Respir Cell Mol Biol
January 2025
The University of Texas Medical Branch at Galveston, Microbiology and Immuology, Galveston, Texas, United States.
Exposure to influenza A virus (IAV), respiratory syncytial virus (RSV), and human metapneumovirus (hMPV) is well-known to increase the risk of pneumonia in humans. Type I interferon (IFN-I) is a hallmark response to acute viral infections, and alveolar macrophages (AMs) constitute the first line of airway defense against opportunistic bacteria. Our study reveals that virus-induced IFN-I receptor (IFNAR1) signaling directly impairs AM-dependent antibacterial protection.
View Article and Find Full Text PDFRegulation of pattern recognition receptor signaling by palmitoylation.
iScience
February 2025
Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Medical University, Xuzhou, Jiangsu, China.
Pattern recognition receptors (PRRs), consisting of Toll-like receptors, RIG-I-like receptors, cytosolic DNA sensors, and NOD-like receptors, sense exogenous pathogenic molecules and endogenous damage signals to maintain physiological homeostasis. Upon activation, PRRs stimulate the sensitization of nuclear factor κB, mitogen-activated protein kinase, TANK-binding kinase 1-interferon (IFN) regulatory factor, and inflammasome signaling pathways to produce inflammatory factors and IFNs to activate Janus kinase/signal transducer and activator of transcription signaling pathways, resulting in anti-infection, antitumor, and other specific immune responses. Palmitoylation is a crucial type of post-translational modification that reversibly alters the localization, stability, and biological activity of target molecules.
View Article and Find Full Text PDFUpregulation of interferon-γ response genes in monocytes and T cells identified by single-cell transcriptomics in patients with anti-citrullinated peptide antibody-positive early rheumatoid arthritis.
Front Immunol
January 2025
The Catholic University of Korea and Ho-Youn Kim's Clinic for Arthritis Rheumatism, Seoul, Republic of Korea.
Introduction: Our aim was to investigate the insufficiently understood differences in the immune system between anti-citrullinated peptide antibody (ACPA)-positive (ACPA) and ACPA-negative (ACPA) early rheumatoid arthritis (eRA) patients.
Methods: We performed multiple cytokine assays using sera from drug-naïve ACPA and ACPA eRA patients. Additionally, we conducted single-cell RNA sequencing of CD45 cells from peripheral blood samples to analyze and compare the distribution and functional characteristics of the cell subsets based on the ACPA status.
Epstein-Barr Virus-Induced 3 Attributes to TLR7-Mediated Splenomegaly.
Immunology
January 2025
Department of Immunology and Molecular Genetics, Kawasaki Medical School, Kurashiki, Japan.
Epstein-Barr virus-induced 3 (EBI3) functions as a component of the heterodimer cytokine IL-27, which regulates innate and acquired immune responses. The expression of EBI3 gene is induced by Toll-like receptors (TLRs). Repeated treatment with imiquimod (IMQ), a TLR7 agonist, induces splenomegaly and cytopaenia due to increased splenic function.
View Article and Find Full Text PDFEarly transcriptional effects of inflammatory cytokines reveal highly redundant cytokine networks.
J Exp Med
April 2025
Department of Immunology, Harvard Medical School, Boston, MA, USA.
Inflammatory cytokines are fundamental mediators of the organismal response to injury, infection, or other harmful stimuli. To elucidate the early and mostly direct transcriptional signatures of inflammatory cytokines, we profiled all immunologic cell types by RNAseq after systemic exposure to IL1β, IL6, and TNFα. Our results revealed a significant overlap in the responses, with broad divergence between myeloid and lymphoid cells, but with very few cell-type-specific responses.
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