Stimulation with glucocorticoids of mouse splenic lymphocytes and peritoneal adherent cells resulted in the formation of a soluble factor--i.e., glycosylation inhibiting factor (GIF)--that inhibits the assembly of N-linked oligosaccharide(s) to IgE-binding factors during their biosynthesis. The major cell sources of GIF are Lyt 2+ I-J+ T cells and macrophages, respectively. The molecular size of GIF from T cells was 15 kDa, while GIF from macrophages consisted of 40- and 15-kDa molecules. GIF from both cell sources bound to monoclonal antibody against lipomodulin and exerted phospholipase inhibitory activity upon dephosphorylation. In view of previous reports that glucocorticoids induce the formation of phospholipase inhibitory protein--i.e., lipomodulin/macrocortin--GIF from T cells and macrophages appear to be phosphorylated derivatives of lipomodulin. GIF released from splenic lymphocytes and macrophages of C57BL/6 mice bound to anti-I-Jb antibodies but not to either anti-I-Jk or anti-I-Js antibodies. Upon stimulation with glucocorticoids, CBA and B10.A(5R) lymphocytes released GIF that bound to anti-I-Jk antibodies but not to anti-I-Jb antibodies, while the same factor from B10.A(3R) lymphocytes bound to anti-I-Jb antibodies. The results indicate that I-J determinants are associated with lipomodulin/macrocortin from T cells and macrophages.
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http://dx.doi.org/10.1073/pnas.83.1.160 | DOI Listing |
J Am Chem Soc
January 2025
Center for Sustainable Materials (SusMat), School of Materials Science and Engineering, Nanyang Technological University, Singapore 639798, Singapore.
Complex coacervation is a form of liquid-liquid phase separation, whereby two types of macromolecules, usually bearing opposite net charges, self-assemble into dense microdroplets driven by weak molecular interactions. Peptide-based coacervates have recently emerged as promising carriers to deliver large macromolecules (nucleic acids, proteins and complex thereof) inside cells. Thus, it is essential to understand their assembly/disassembly mechanisms at the molecular level in order to tune the thermodynamics of coacervates formation and the kinetics of cargo release upon entering the cell.
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Institute for Clinical Chemistry and Laboratory Medicine, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Fetscherstrasse 74, 01307, Dresden, Germany.
Metabolic flexibility is key for the function of myeloid cells. Arginine metabolism is integral to the regulation of myeloid cell responses. Nitric oxide (NO) production from arginine is vital for the antimicrobial and pro-inflammatory responses.
View Article and Find Full Text PDFOncogene
January 2025
Department of Gastroenterology, Endocrinology and Metabolism, Center for Tumor and Immune Biology, Philipps University Marburg, Marburg, Germany.
The development of resistance remains one of the biggest challenges in clinical cancer patient care and it comprises all treatment modalities from chemotherapy to targeted or immune therapy. In solid malignancies, drug resistance is the result of adaptive processes occurring in cancer cells or the surrounding tumor microenvironment (TME). Future therapy attempts will therefore benefit from targeting both, tumor and stroma compartments and drug targets which affect both sides will be highly appreciated.
View Article and Find Full Text PDFApoptosis
January 2025
Department of Cardiac Surgery, First Affiliated Hospital of Sun Yat-sen University, 58 Zhongshan II Rd, Guangzhou, 510080, China.
Recent studies have suggested that sVEGFR3 is involved in cardiac diseases by regulating lymphangiogenesis; however, results are inconsistent. The aim of this study was to investigate the function and mechanism of sVEGFR3 in myocardial ischemia/reperfusion injury (MI/RI). sVEGFR3 effects were evaluated in vivo in mice subjected to MI/RI, and in vitro using HL-1 cells exposed to oxygen-glucose deprivation/reperfusion.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Biomedical Engineering, University of Rochester, Rochester, NY, USA.
The aberrant vascular response associated with tendon injury results in circulating immune cell infiltration and a chronic inflammatory feedback loop leading to poor healing outcomes. Studying this dysregulated tendon repair response in human pathophysiology has been historically challenging due to the reliance on animal models. To address this, our group developed the human tendon-on-a-chip (hToC) to model cellular interactions in the injured tendon microenvironment; however, this model lacked the key element of physiological flow in the vascular compartment.
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