- Immune cells in cancer
- Phagocytosis and Immune Regulation
- Galectins and Cancer Biology
- Endoplasmic Reticulum Stress and Disease
- Adipokines, Inflammation, and Metabolic Diseases
- Biomarkers in Disease Mechanisms
- Cancer-related gene regulation
- Immune Response and Inflammation
- Atherosclerosis and Cardiovascular Diseases
- Kruppel-like factors research
- Immune responses and vaccinations
- Lipoproteins and Cardiovascular Health
- Cancer, Lipids, and Metabolism
- Heterotopic Ossification and Related Conditions
- IL-33, ST2, and ILC Pathways
- Genetic Syndromes and Imprinting
- Inflammasome and immune disorders
- Peptidase Inhibition and Analysis
- Diabetes and associated disorders
- Inflammation biomarkers and pathways
University of Oxford
2023
University of Sheffield
2016-2020
Singapore Immunology Network
2020
Agency for Science, Technology and Research
2020
Abstract Monocytes play a central role in regulating inflammation response to infection or injury, and during auto-inflammatory diseases. Human blood contains classical, intermediate non-classical monocyte subsets that each express characteristic patterns of cell surface CD16 CD14; subset also has specific functional properties, but the mechanisms underlying many their distinctive features are undefined. Of particular interest is how regulate secretion apical pro-inflammatory cytokine IL-1β,...
Trib1 controls atherosclerotic plaque macrophage function by up-regulating OLR1, promoting foam cell formation and atherosclerosis.
ABSTRACT Heterotopic ossification (HO) is bone formation that occurs after trauma within tissues do not normally have the property of ossification, resulting in pain and disability. The genetic architecture HO remains unclear. In first genome-wide association studies this disease, we identify human-only long non-coding RNA-encoding gene CASC20 as a robust, replicating susceptibility locus for KIF26B potential severity locus. We find both are expressed human bone. Both expression upregulated...
Abstract Macrophages drive atherosclerotic plaque progression and rupture, hence attenuating their atherosclerosis-inducing properties holds promise for reducing coronary heart disease (CHD). Recent studies in mouse models have demonstrated that Tribbles 1 (Trib1) regulates macrophage phenotype shows Trib1 deficiency increases plasma cholesterol triglyceride levels, suggesting reduced TRIB1 expression mediates the strong genetic association between locus increased CHD risk man. However, we...
<h3>Rationale</h3> Cardiovascular disease is the leading cause of death world–wide. Macrophages are crucial in regulating plaque environment, especially lipid content. However, current characterisation macrophage phenotypes lipoprotein handling capacity conflicting and incomplete. We hypothesised that differed among distinct due to differential gene protein expression. tested this using a range functional, expression assays. <h3>Methodology</h3> Monocytes were isolated from healthy donor...