The chemokine receptor CXCR3 is expressed on immune cells to co-ordinate lymphocyte activation and migration. CXCR3 binds three chemokine ligands, CXCL9, CXCL10 and CXCL11. These ligands display distinct expression patterns and ligand signaling biases; however, how each ligand functions individually and collaboratively is incompletely understood. CXCL9 and CXCL10 are considered pro-inflammatory chemokines during viral infection, while CXCL11 may induce a tolerizing state. The investigation of the individual role of CXCL11 in vivo has been hampered as C57BL/6 mice carry several mutations that result in a null allele. Here, CRISPR/Cas9 was used to correct these mutations on a C57BL/6 background. It was validated that CXCL11 mice expressed CXCL11 protein in dendritic cells, spleen and lung. CXCL11 mice were largely phenotypically indistinguishable from C57BL/6 mice, both at steady-state and during two models of viral infection. While CXCL11 expression did not modify acute antiviral responses, this study provides a new tool to understand the role of CXCL11 in other experimental settings.
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http://dx.doi.org/10.1111/imcb.12541 | DOI Listing |
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
January 2025
Department of Neurosurgery, Wuhan NO.1 Hospital, Wuhan 432000, China. *Corresponding author, E-mail:
Objective To investigate the effects and molecular mechanism of Homer protein homolog 1a (Homer 1a) overexpression on nerve injury in mice with traumatic brain injury (TBI). Methods Sixty male C57BL/6 mice were randomly divided into five groups: sham group, TBI group, empty lentivirus (Lv-NC) group, Homer 1a overexpression lentivirus (Lv-Homer 1a) group and Lv-Homer 1a + 740 Y-P group, with 12 mice in each group. The lentivirus was orthotopic injected into the cerebral cortex of mice 5 d before modeling, while 740 Y-P was injected intraperitoneally 1 d before modeling.
View Article and Find Full Text PDFCell Signal
January 2025
Department of Cardiovascular Surgery, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China. Electronic address:
Pulmonary artery hypertension (PAH) is characterized by a cancer-like metabolic shift towards aerobic glycolysis. Nuclear Receptor Binding SET Domain Protein 2 (NSD2), a histone methyltransferase, has been implicated in PAH, yet its precise role remains unclear. In this study, we induced PAH in C57BL/6 mice using monocrotaline (MCT) and observed increased FOLR1 expression in PAH tissues, which was suppressed by NSD2 knockdown.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Division of Endocrinology, Tongji Hospital, Huazhong University of Science & Technology, Wuhan, 430030, PR China; Branch of National Clinical Research Center for Metabolic Diseases, Hubei, PR China. Electronic address:
Recent studies demonstrated that glucagon-like peptide-1 receptor agonists (GLP-1RA) have promising prospects in promoting wound healing. In this study, we intend to investigate the pro-healing effect and potential molecular mechanism of topical administration of GLP-1RA liraglutide on wounds in normoglycemic mice. Two full-thickness wounds were created on the back of the C57BL/6 mice.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Biopharmaceutical Lab, College of Life Science, Northeast Agricultural University, Harbin 150030, China; Research Center of Genetic Engineering of Pharmaceuticals of Heilongjiang Province, Northeast Agricultural University, Harbin 150030, China; Key Laboratory of Agricultural Biological Functional Gene, Northeast Agricultural University, Harbin 150030, China. Electronic address:
Background: The blood FGF21 expression has been previously suggested to increase in patients developing atopic dermatitis (AD) and asthma. However, its impact on atopic march is rarely analyzed. The present work focused on investigating the role of Fibroblast Growth Factor 21(FGF21) in atopic march mice and its underlying mechanisms.
View Article and Find Full Text PDFVaccine
January 2025
Vaxine Pty Ltd, Warradale, Adelaide, SA 5046, Australia; Australian Respiratory and Sleep Medicine Institute Ltd, Adelaide, SA 5042, Australia. Electronic address:
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