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In a study by Benkoucha et al., HGF exerted an anti-inflammatory effect through the generation of tolerogenic dendritic cells with the consequent suppression of auto-reactive T helper cells 1 (Th1) and Th17 cells and leading to the reduction of CD4 + T-cell-mediated nervous system injury in the experimental autoimmune encephalomyelitis (EAE) animal model of MS, in which HGF was overexpressed (HGF transgenic mice) ( in vitro ( On the basis of these studies, the capacity of HGF to modulate neuro-inflammation is thus associated with an alteration in the balance of pro-inflammatory (Th1 and Th17) and anti-inflammatory (Th2 and Tregs) CD4 + T cells by influencing dendritic cell function

Interactions between c-MET II and HGF I Distinct to the binding mode between c-MET I and HGF I that involves multiple domains of HGF, only the K1 domain located on the opposite side of HGF I makes direct contact with c-MET II, indicating that HGF-K1 is essential for c-MET activation (Fig