- 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.
HMGB1 concentration measurements in trauma patients: assessment of pre-analytical conditions and sample material
Mol Med, 26 (1), 5
Hypo-osmotic Stress Drives IL-33 Production in Human Keratinocytes-An Epidermal Homeostatic Response
J Invest Dermatol, 139 (1), 81-90
Inhibition of Endothelial NOTCH1 Signaling Attenuates Inflammation by Reducing Cytokine-Mediated Histone Acetylation at Inflammatory Enhancers
Arterioscler Thromb Vasc Biol, 38 (4), 854-869