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A novel ex vivo approach for investigating profibrotic macrophage polarization using murine precision-cut lung slices.
Biochem Biophys Res Commun
December 2024
Firestone Institute for Respiratory Health, Department of Medicine, McMaster University and the Research Institute of St. Joe's Hamilton, 50 Charlton Avenue East, Hamilton, Ontario, L8N 4A6, Canada; McMaster Immunology Research Centre, Department of Medicine, McMaster University, 1280 Main Street West, Hamilton, Ontario, L8S 4L8, Canada. Electronic address:
Article Synopsis
- Idiopathic pulmonary fibrosis (IPF) is a severe lung disease marked by excessive scarring, leading to poor respiratory function and a need for new treatment strategies, particularly involving macrophages, the key immune cells in the lungs.
- The study aimed to explore macrophage behavior in lung slices (PCLS), which are real lung tissues cultured in a lab, to better replicate the lung environment compared to isolated cells in vitro.
- Results showed that a polarization cocktail of specific cytokines can induce macrophage markers related to lung fibrosis in PCLS without harming the tissue, demonstrating a promising model for studying macrophage roles in IPF.
Efficacy of LCMV-based cancer immunotherapies is unleashed by intratumoral injections of polyI:C.
J Immunother Cancer
April 2024
Program of Immunology and Immunotherapy, Cima Universidad de Navarra, Pamplona, Spain
Background: Lymphocytic choriomeningitis virus (LCMV) belongs to the Arenavirus family known for inducing strong cytotoxic T-cell responses in both mice and humans. LCMV has been engineered for the development of cancer immunotherapies, currently undergoing evaluation in phase I/II clinical trials. Initial findings have demonstrated safety and an exceptional ability to activate and expand tumor-specific T lymphocytes.
View Article and Find Full Text PDFMacrophage Activation in Synovitis and Osteoarthritis of Temporomandibular Joint and Its Relationship with the Progression of Synovitis and Bone Remodeling.
Am J Pathol
February 2024
Department of Oral and Maxillofacial Surgery, School and Hospital of Stomatology, Wuhan University, Wuhan, China. Electronic address:
This study investigates the regulatory mechanisms of synovial macrophages and their polarization in the progression of temporomandibular joint osteoarthritis (TMJOA). Macrophage depletion models were established by intra-articular injection of clodronate liposomes and unloaded liposomes. TMJOA was induced by intra-articular injection of 50 μL Complete Freund's Adjuvant and the surgery of disc perforation.
View Article and Find Full Text PDFEvolocumab prevents atrial fibrillation in rheumatoid arthritis rats through restraint of PCSK9 induced atrial remodeling.
J Adv Res
July 2024
Department of Cardiology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China; NHC Key Laboratory of Cell Translation, Harbin Medical University, Heilongjiang 150001, China; Key Laboratory of Hepatosplenic Surgery, Harbin Medical University, Ministry of Education, Harbin 150001, China; Key Laboratory of Cardiac Diseases and Heart Failure, Harbin Medical University, Harbin 150001, China; Heilongjiang Key Laboratory for Metabolic Disorder & Cancer Related Cardiovascular Diseases, Harbin 150081, China; Institute of Metabolic Disease, Heilongjiang Academy of Medical Science, Harbin, China. Electronic address:
Introduction: Proprotein convertase subtilisin/kexin type 9 (PCSK9) is implicated in the pathogenesis and progression of autoimmune disease. Patients with rheumatoid arthritis (RA) are at high risk of developing atrial fibrillation (AF), while whether PCSK9 is involved in the onset of AF among RA patients remains unclear.
Objectives: To explore the role of PCSK9 in the occurrence of AF in RA patients and decipher the underlying mechanism.
Fibroblast-derived PI16 sustains inflammatory pain via regulation of CD206 myeloid cells.
Brain Behav Immun
August 2023
Laboratories of Neuroimmunology, Department of Symptom Research, Division of Internal Medicine, University of Texas MD Anderson Cancer Center, Houston, TX, United States. Electronic address:
Originally identified in fibroblasts, Protease Inhibitor (PI)16 was recently shown to be crucial for the development of neuropathic pain via effects on blood-nerve barrier permeability and leukocyte infiltration, though its impact on inflammatory pain has not been established. Using the complete Freund's Adjuvant inflammatory pain model, we show that Pi16 mice are protected against sustained inflammatory pain. Accordingly, intrathecal delivery of a PI16 neutralizing antibody in wild-type mice prevented sustained CFA pain.
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