A5005325608- Complement system in diseases
- Asthma and respiratory diseases
- Inhalation and Respiratory Drug Delivery
- Monoclonal and Polyclonal Antibodies Research
- Immune responses and vaccinations
- Immune Cell Function and Interaction
- Mast cells and histamine
- Immunotherapy and Immune Responses
- CAR-T cell therapy research
- SARS-CoV-2 and COVID-19 Research
- Allergic Rhinitis and Sensitization
- IL-33, ST2, and ILC Pathways
- Inflammation biomarkers and pathways
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Inflammasome and immune disorders
- Neonatal Respiratory Health Research
- Adenosine and Purinergic Signaling
- Pleural and Pulmonary Diseases
- Electrolyte and hormonal disorders
- Urticaria and Related Conditions
- Food Allergy and Anaphylaxis Research
- Renal Diseases and Glomerulopathies
- Autoimmune Bullous Skin Diseases
- Immunodeficiency and Autoimmune Disorders
- Hormonal Regulation and Hypertension
University of Lübeck
2011-2025
Cincinnati Children's Hospital Medical Center
2010-2025
University Hospital Schleswig-Holstein
2024
Institute for Integrative and Experimental Genomics
2018
University of Cincinnati
2010
Boston Children's Hospital
2005
The anaphylatoxic peptide C3a is part of a basic immunological defense mechanism, the complement system. Research on human receptor and signal transduction hampered by lack suitable cell or line. We screened tumor lines blood cells for C3a-dependent increase in cytosolic Ca2+ ([Ca2+]i) analyzed this reaction fura-2/AM fluorescence assay suspension. U937 cells, when differentiated with dibutyryl-cAMP (Bt2cAMP), purified neutrophils reacted dose-dependent fashion to analogue synthetic peptide....
Microbial exposure at barrier interfaces drives development and balance of the immune system, but consequences local infections for systemic immunity secondary inflammation are unclear. Here, we show that skin to bacterium Staphylococcus aureus persistently shapes system mice with specific impact on progenitor mature bone marrow neutrophil eosinophil populations. The infection-imposed changes in eosinophils were long-lasting associated functional as well imprinted epigenetic metabolic...
The complement system is an ancient part of innate immunity sensing highly pathogenic coronaviruses by Mannan-binding lectin resulting in pathway-activation and subsequent generation the anaphylatoxins (AT) C3a C5a as important effector molecules. Complement deposition endothelial cells high blood serum levels have been reported COVID-19 patients with severe illness, suggesting vigorous activation leading to systemic thrombotic microangiopathy (TMA). Strikingly, SARS-CoV-2-infected African...
Abstract Because the complement activation products C3a and C5a can induce anaphylaxis by activating mast cells, basophils, macrophages, neutrophils other cell types, we hypothesized that murine mediated a complement-activating antibody isotype would be less severe in mice deficient receptors for these anaphylatoxins or central component, C3, than wild-type mice. Surprisingly, isotype, IgG2a, was considerably more C3 both C3aR C5aR; with approximately twice drop body temperature mutant as on...
Auto-antibodies (AAbs) drive undesired inflammation mainly through joint activation of IgG Fc receptors (FcγRs) and the complement system. The latter results in generation powerful chemoattractant pro-inflammatory mediator C5a. In experimental models auto-immune such as rheumatoid arthritis, SLE skin blistering diseases, we others have previously shown that C5a drives accumulation neutrophils inflammatory monocytes. Epidermolysis Bullosa Acquisita (EBA), a subepidermal disease caused by AAbs...
Deposition of antigen‐antibody complexes in tissues is a hallmark autoimmune diseases such as rheumatoid arthritis. Mice lacking FcγRs for complexed IgG (γ‐chain deficient, γ −/− ) or complement components are protected from developing arthritis and mast cells vascular permeability required disease. However, these studies may not fully reflect human inflammation mouse structurally differ. Here we show that neutrophil‐selective transgenic expression the uniquely FcγRIIA mice was sufficient to...
Abstract Food-induced anaphylaxis is a serious allergic reaction mainly caused by antigen cross-linking of IgE-loaded Fce-receptors on mast cells (MCs). Such MC activation leads to the release pro-inflammatory mediators which results in manifestation disease. Here, we demonstrate that complement fragment C5a plays an important and until now not recognized role development severity food allergy. We subjected C5aR1−/− wild-type (wt) Balb/c mice oral ovalbumin (OVA)-induced anaphylaxis....