Injection of mice with endotoxin results in the formation of auto-antibodies and the appearance of soluble immune complexes in the blood. In this study the relationship between the production and serum levels of autohaemolysins and circulating immune complex titres was investigated. Immune complexes were detected by a solid-phase C1q-binding assay and found to contain antibodies of the IgM, but not of the IgG class. Individual mice showed marked differences as to their splenic plaque-forming cells, serum autohaemolysin, and circulating immune complex responses, both in kinetic studies and dose-response experiments. The dissociation between production and serum levels of auto-antibodies was ascribed to extrasplenic synthesis or a disproportionate production per plasma cell. The independent behaviour of the circulating immune complex response could, at least partially, be attributed to differential complement-dependent clearance from the circulation. The implications of our findings for the laboratory diagnosis of auto-immunity at the blood level are being discussed.
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Front Immunol
January 2025
Team Immunity and Cancer, Cancer Research Center of Marseille (CRCM), Inserm U1068, CNRS UMR7258, Paoli-Calmettes Institute, University of Aix-Marseille UM105, Marseille, France.
Introduction: Acute myeloid leukemia (AML) is a rare haematological cancer with poor 5-years overall survival (OS) and high relapse rate. Leukemic cells are sensitive to Natural Killer (NK) cell mediated killing. However, NK cells are highly impaired in AML, which promote AML immune escape from NK cell immune surveillance.
View Article and Find Full Text PDFJ Exp Biol
January 2025
1School of Natural Sciences, Brambell Laboratories, Bangor University, Bangor, Gwynedd LL57 2UW, UK.
The allatostatin (AST) family of neuropeptides are widespread in arthropods. The multitude of structures and pleiotropic actions reflect the tremendous morphological, physiological and behavioral diversity of the phylum. Regarding the AST-C (with C-terminal PISCF motif) peptides, crustaceans commonly express three (AST-C, -CC, -CCC) that have likely arisen by gene duplication.
View Article and Find Full Text PDFCardiol Young
January 2025
Adult Congenital Heart Centre and National Centre for Pulmonary Hypertension, Royal Brompton and Harefield Hospitals, Guy's and St Thomas's NHS Foundation Trust, Imperial College, London, UK.
We present the case of a 31-year-old female with Fontan circulation who developed signs of protein-losing enteropathy 10 days after second COVID-19 vaccination. After standard investigations for identification of potential triggers for protein-losing enteropathy, we concluded that coronavirus disease 2019 (COVID-19) booster vaccination could have been the most probable underlying trigger. Prompt investigation of new symptoms post-vaccination in high-risk patients is necessary.
View Article and Find Full Text PDFNat Commun
January 2025
School of Disaster and Emergency Medicine, Faculty of Medicine, Tianjin University, No. 92 Weijin Road, Nankai District, Tianjin, 300072, China.
Rhabdomyolysis or Crush syndrome-related AKI (RM/CS-AKI) has high mortality, and there is no effective early on-site treatment method. The critical pathogenic factor of RM/CS-AKI is the excessive free myoglobin (Mb) in blood circulation. Here, based on the concept of creating a "mobile barrier", we develop an anti-Mb rabbit monoclonal antibody (RabMAb) with high specificity, affinity, stability, and broad species reactivity.
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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