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(hämtat ur Lunds universitets publikationsdatabas)
- Platelet-derived S100A8/A9 and cardiovascular disease in systemic lupus erythematosus.
- The assessment of serum-mediated phagocytosis of necrotic material by polymorphonuclear leukocytes to diagnose and predict the clinical features of systemic lupus erythematosus: an observational longitudinal study
- A subset of patients with systemic lupus erythematosus fails to degrade DNA from multiple clinically relevant sources.
- Circulating complexes between tumour necrosis factor-alpha and etanercept predict long-term efficacy of etanercept in juvenile idiopathic arthritis.
- Type I interferon-mediated skewing of the serotonin synthesis is associated with severe disease in systemic lupus erythematosus.
- Low production of reactive oxygen species in granulocytes is associated with organ damage in systemic lupus erythematosus
- Platelet activation and anti-phospholipid antibodies collaborate in the activation of the complement system on platelets in systemic lupus erythematosus.
- Serum from patients with systemic vasculitis induces alternatively activated macrophage M2c polarization.
- Combination of Autoantibodies Against Different Histone Proteins Influences Complement-dependent Phagocytosis of Necrotic Cell Material by Polymorphonuclear Leukocytes in Systemic Lupus Erythematosus.
- IgG glycan hydrolysis by EndoS diminishes the pro-inflammatory properties of immune complexes from patients with SLE - a possible new treatment?
- IgG glycan hydrolysis by endoglycosidase S diminishes the proinflammatory properties of immune complexes from patients with systemic lupus erythematosus: A possible new treatment?
- Increased C1q, C4 and C3 deposition on platelets in patients with systemic lupus erythematosus - a possible link to venous thrombosis?
- Increased IgG on cell-derived plasma microparticles in systemic lupus erythematosus is associated with autoantibodies and complement activation.
- Neutrophil Extracellular Traps That Are Not Degraded in Systemic Lupus Erythematosus Activate Complement Exacerbating the Disease.
- Vaccination against encapsulated bacteria in hereditary C2 deficiency results in antibody response and opsonization due to antibody-dependent complement activation.
- Apoptosis of Peripheral Blood Leukocytes in Systemic Lupus Erythematosus: Studies on Serum Induction and Complement-Dependent Clearance Mechanisms
- Homozygosity For a Novel Mutation in the C1q C Chain Gene in a Turkish Family With Hereditary C1q Deficiency
- Platelet transcriptional profile and protein expression in patients with systemic lupus erythematosus: up-regulation of the type I interferon system is strongly associated with vascular disease.
- Recombinant human complement component C2 produced in a human cell line restores the classical complement pathway activity in-vitro: an alternative treatment for C2 deficiency diseases
- C1q Inhibits Immune Complex-Induced Interferon-alpha Production in Plasmacytoid Dendritic Cells A Novel Link Between C1q Deficiency and Systemic Lupus Erythematosus Pathogenesis
- C1q inhibits immune complex induced IFN-alpha production in plasmacytoid dendritic cells-A novel link between C1q deficiency and SLE pathogenesis
- Complement classical pathway components are all important in clearance of apoptotic and secondary necrotic cells.
- Influence of IgG allotypes on defense against Haemophilus influenzae type b in children-A complement-dependent mechanism?
- Complement classical pathway components are all important in clearance of apoptotic cells
- Role of C1q in regulation of IFN-alpha production
- SLE serum induces classical caspase-dependent apoptosis independent of death receptors
- Serum bactericidal activity against Neisseria meningitidis in patients with C3 nephritic factors is dependent on IgG allotypes.
- Characterization of non-expressed C4 genes in a case of complete C4 deficiency: identification of a novel point mutation leading to a premature stop codon
- Expression of properdin in complete and incomplete deficiency: normal in vitro synthesis by monocytes in two cases with properdin deficiency type II due to distinct mutations