MET is required for the recruitment of anti-tumoural neutrophils

During cancer or infections, the release of cytokines such as IL-1 at the inflammatory site will promote the expression of TNF-α on the endothelium and the surrounding tissue. When circulating neutrophils will encounter the activated endothelium, TNF-α will unleash NF-κB through the binding to TNFR1, which in turn will induce MET expression on neutrophil surface. HGF, also released and proteolytically activated at the site of inflammation, will bind to MET and stimulate the firm adhesion of neutrophils to the endothelium, likely via integrin engagement, and thus neutrophil diapedesis. Once extravasated, HGF/MET pathway will still function on neutrophils by reinforcing their cytotoxic response through the induction of iNOS and NO production, ultimately favouring a bactericidal and tumouricidal neutrophil phenotype.

Publication

MET is required for the recruitment of anti-tumoural neutrophils. (2015) Veronica Finisguerra, et al. Nature. 2015 Jun 18;522(7556):349-353. Figure: F1. All organisms Homo sapiens Mus musculus Drosophila melanogaster

Disease mentions