- Systemic Lupus Erythematosus Research
- interferon and immune responses
- Immune Response and Inflammation
- Antimicrobial Peptides and Activities
- Cytokine Signaling Pathways and Interactions
- Peripheral Neuropathies and Disorders
- Immunotherapy and Immune Responses
- Multiple Sclerosis Research Studies
- Atherosclerosis and Cardiovascular Diseases
- Viral Infections and Immunology Research
- Complement system in diseases
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Skin and Cellular Biology Research
- Renal Diseases and Glomerulopathies
- DNA Repair Mechanisms
- Immune Cell Function and Interaction
- RNA regulation and disease
- Protein Tyrosine Phosphatases
- Ubiquitin and proteasome pathways
- Neuroinflammation and Neurodegeneration Mechanisms
- Polyomavirus and related diseases
- Inflammasome and immune disorders
- Immune responses and vaccinations
- T-cell and B-cell Immunology
- Mitochondrial Function and Pathology
University of Edinburgh
2015-2024
UK Dementia Research Institute
2018-2024
Institute of Genetics and Cancer
2015-2019
Medical Research Council
2016-2019
University of Cambridge
2017
University of Lincoln
2017
Type I interferons (IFNs) are essential mediators of antiviral responses. These cytokines have been implicated in the pathogenesis autoimmunity, most notably systemic lupus erythematosus (SLE), diabetes mellitus, and dermatomyositis, as well monogenic type interferonopathies. Despite a fundamental role health disease, direct quantification IFNs has challenging. Using single-molecule array (Simoa) digital ELISA technology, we recorded attomolar concentrations IFNα healthy donors, viral...
Human β-defensin 3 (hBD3) is a cationic antimicrobial peptide with potent bactericidal activity in vitro. HBD3 produced response to pathogen challenge and can modulate immune responses. The amplified recognition of self-DNA by human plasmacytoid dendritic cells has been previously reported, but we show here that hBD3 preferentially enhances the bacterial DNA mouse Flt-3 induced (FLDCs) peripheral blood mononuclear cells. We effect mediated through TLR9 although significantly increases...
Human β-defensin 3 (hBD3) is a cationic host defence peptide and part of the innate immune response. HBD3 present on highly copy number variable block six genes, increased associated with autoimmune disease psoriasis. It not known how this increase influences development, but psoriasis T cell-mediated activation system required for initial trigger that leads to amplification stage. We investigated effect hBD3 response primary macrophages various TLR agonists. exacerbated production type I...
<ns4:p><ns4:bold>Background:</ns4:bold> Monoallelic and biallelic mutations in the exonuclease <ns4:italic>TREX1</ns4:italic> cause monogenic small vessel diseases (SVD). Given recent evidence for genetic pathophysiological overlap between polygenic forms of SVD, evaluation stroke is warranted.</ns4:p><ns4:p> <ns4:bold>Methods:</ns4:bold> We sequenced gene an exploratory cohort patients with lacunar (Edinburgh Stroke Study, n=290 cases). subsequently performed a fully blinded case-control...
ABSTRACT Introduction Type I interferons are cytokines involved in innate immunity against viruses. Genetic disorders of type interferon regulation associated with a range autoimmune and cerebrovascular phenotypes. Carriers pathogenic variants genetic generally considered asymptomatic. Preliminary data suggests, however, that genetically determined dysregulation responses is autoimmunity, may also be relevant to sporadic disease dementia. We aim determine whether functional genes signalling...
Type I interferons are cytokines involved in innate immunity against viruses. Genetic disorders of type interferon regulation associated with a range autoimmune and cerebrovascular phenotypes. Carriers pathogenic variants genetic generally considered asymptomatic. Preliminary data suggests, however, that genetically determined dysregulation responses is autoimmunity, may also be relevant to sporadic disease dementia. We aim determine whether functional genes signalling the risk stroke,...