A5086672334- Cell Adhesion Molecules Research
- Immune cells in cancer
- Immune Response and Inflammation
- Immune responses and vaccinations
- Diabetes and associated disorders
- Immune Cell Function and Interaction
- Adipokines, Inflammation, and Metabolic Diseases
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Blood Coagulation and Thrombosis Mechanisms
- Cancer, Hypoxia, and Metabolism
- Liver Disease Diagnosis and Treatment
- Protease and Inhibitor Mechanisms
- Acute Myeloid Leukemia Research
- Angiogenesis and VEGF in Cancer
- Adipose Tissue and Metabolism
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Platelet Disorders and Treatments
- Hematopoietic Stem Cell Transplantation
- Phagocytosis and Immune Regulation
- Pancreatic function and diabetes
- Advanced Glycation End Products research
- S100 Proteins and Annexins
- Erythrocyte Function and Pathophysiology
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Hormonal Regulation and Hypertension
Technische Universität Dresden
2016-2025
Paul Langerhans Institute Dresden
2014-2025
University Hospital Carl Gustav Carus
2016-2025
Deutsches Diabetes-Zentrum e.V.
2016-2025
National Center for Tumor Diseases
2018-2025
German Center for Diabetes Research
2016-2025
Heinrich Heine University Düsseldorf
2016-2025
The Queen's Medical Research Institute
2019-2024
University of Edinburgh
2019-2024
Helmholtz Zentrum München
2018-2023
Trained innate immunity fosters a sustained favorable response of myeloid cells to secondary challenge, despite their short lifespan in circulation. We thus hypothesized that trained acts via modulation hematopoietic stem and progenitor (HSPCs). Administration β-glucan (prototypical trained-immunity-inducing agonist) mice induced expansion progenitors the lineage, which was associated with elevated signaling by immune mediators, such as IL-1β granulocyte-macrophage colony-stimulating factor...
The pattern recognition receptor, RAGE (receptor for advanced glycation endproducts), propagates cellular dysfunction in several inflammatory disorders and diabetes. Here we show that functions as an endothelial adhesion receptor promoting leukocyte recruitment. In animal model of thioglycollate-induced acute peritonitis, recruitment was significantly impaired RAGE-deficient mice opposed to wild-type mice. diabetic observed enhanced the inflamed peritoneum compared with nondiabetic mice;...
Trained innate immunity, induced via modulation of mature myeloid cells or their bone marrow progenitors, mediates sustained increased responsiveness to secondary challenges. Here, we investigated whether anti-tumor immunity can be enhanced through induction trained immunity. Pre-treatment mice with β-glucan, a fungal-derived prototypical agonist resulted in diminished tumor growth. The effect β-glucan-induced was associated transcriptomic and epigenetic rewiring granulopoiesis neutrophil...
The recently described junctional adhesion molecules (JAMs) in man and mice are involved homotypic heterotypic intercellular interactions. Here, a third member of this family, human JAM-3, was identified as novel counterreceptor on platelets for the leukocyte β2-integrin Mac-1 (αMβ2, CD11b/CD18). With help two monoclonal antibodies, Gi11 Gi13, against 43-kD surface glycoprotein platelets, full-length cDNA encoding JAM-3 identified. is type I transmembrane containing Ig-like domains. Although...
Sepsis is a frequently fatal condition characterized by an uncontrolled and harmful host reaction to microbial infection. Despite the prevalence severity of sepsis, we lack fundamental grasp its pathophysiology. Here report that cytokine interleukin-3 (IL-3) potentiates inflammation in sepsis. Using mouse model abdominal showed innate response activator B cells produce IL-3, which induces myelopoiesis Ly-6C(high) monocytes neutrophils fuels storm. IL-3 deficiency protects mice against In...
Endothelial progenitor cells (EPCs) are recruited to ischemic regions and improve neovascularization. Integrins contribute EPC homing. High-mobility group box 1 (HMGB1) is a nuclear protein that released extracellularly on cell necrosis tissue damage, eliciting proinflammatory response stimulating repair. In the present study, we investigated effects of HMGB1 EPCs express receptors RAGE (receptor for advanced glycation end products) TLR2 (Toll-like receptor 2). migration was stimulated by in...
Leukocyte recruitment to sites of infection or inflammation requires multiple adhesive events. Although numerous players promoting leukocyte-endothelial interactions have been characterized, functionally important endogenous inhibitors leukocyte adhesion not identified. Here we describe the endothelially derived secreted molecule Del-1 (developmental endothelial locus–1) as an anti-adhesive factor that interferes with integrin LFA-1–dependent adhesion. Endothelial deficiency increased in...
Inflammatory bone loss from periodontal infections in leukocyte adhesion deficiency disease can be reversed by treatment with antibodies to IL-17 or IL-23.
Breaching endothelial cells (ECs) is a decisive step in the migration of leukocytes from vascular lumen to extravascular tissue, but fundamental aspects this response remain largely unknown. We have previously shown that neutrophils can exhibit abluminal-to-luminal through EC junctions within mouse cremasteric venules and elicited following reduced expression and/or functionality junctional adhesion molecule-C (JAM-C). Here we demonstrate lipid chemoattractant leukotriene B4 (LTB4) was...
The tuberculosis vaccine bacillus Calmette-Guérin (BCG) protects against some heterologous infections, probably via induction of non-specific innate immune memory in monocytes and natural killer (NK) cells, a process known as trained immunity. Recent studies have revealed that the immunity is associated with bias toward granulopoiesis bone marrow hematopoietic progenitor but it unknown whether BCG vaccination also leads to functional reprogramming mature neutrophils. Here, we show healthy...