Our science
What we study
There is exquisite control of immune cell recruitment to all bodily tissues. In injury and disease, such control is important to appropriately resolve the insult or infection whilst limiting inflammation that can drive pathology. Chemokines mediate immune cell recruitment and are heavily implicated in pathological inflammation — but have not been successfully therapeutically targeted, due to limited understanding of their basic biology. We believe the glycocalyx holds the answer.
CXCL4
recruits immune cells via proteoglycans, not chemokine receptors
HS
glycocalyx on leukocytes regulates their own recruitment
GAGs
decode complex multi-chemokine signals in disease
BBB
heparan sulfate mediates CXCL4 transport across the blood-brain barrier
The glycocalyx as a physical regulator of immune recruitment
The glycocalyx on endothelial and immune cells physically regulates the molecular interactions required for leukocyte recruitment into inflamed tissues. We are defining how its structure and composition gate the adhesion cascade during inflammation — including how the leukocyte's own glycocalyx controls its recruitment.
Proteoglycans as chemokine receptors
Proteoglycans within the glycocalyx can act directly as chemokine receptors, driving immune cell recruitment during pathological inflammation independently of canonical GPCRs. Our Cell Reports paper demonstrated that CXCL4 mediates widespread leukocyte recruitment entirely through extracellular matrix proteoglycans. This fundamentally reframes chemokine biology.
Glycocalyx remodelling in disease
We study how the glycocalyx is remodelled during inflammation, viral infection, and ageing — and what consequences this has for chemokine signalling, immune cell trafficking, and tissue homeostasis across organs including skin, lung, brain, and peritoneum.
