- We have discovered that inhibition of endothelial Notch signalling attenuates inflammation and we now show that selective inhibition of two Notch receptors inhibits murine arthritis. We are now generating recombinant human antibodies to these receptors with a selective ligand-neutralizing profile that will be subject to preclinical trials.
- We have generated IL-33-deficient rats by means of CRISPR/Cas9 technology, mice a completely different regulation and expression pattern when compared man and most other mammals including the rat. We reveal interesting responses in a model of endotoxemian designed to resemble sepsis.
- We have discovered that IL-33 modulates the differentiation of fibroblast during experimental kidney fibrosis.
- We have discovered that IL-33 is induced by hypoosmosis in human keratinocytes, viewing this as an epidermal homeostatic response.
A novel somatic mutation in GNB2 provides new insights to the pathogenesis of Sturge-weber syndrome
Hum Mol Genet (in press)
Inflammatory activation of endothelial cells increases glycolysis and oxygen consumption despite inhibiting cell proliferation
FEBS Open Bio, 11 (6), 1719-1730
Targeting the Notch Signaling Pathway in Chronic Inflammatory Diseases
Front Immunol, 12, 668207