HMGB1: An Active “Go-Between” Linking Innate and Adaptive Immunity
Considering the contribution of HMGB1 to inflammation, a considerable amount of work has been done to define its effect on immune cells. Independently from the mechanism responsible for its release (active secretion or passive diffusion outside a necrotic cells), HMGB1 has been shown to participate to the recruitment of inflammatory cells to the site of the “danger”.
Then, it takes part to an active cross-talk between natural killers cells (NKs), dendritic cells (DCs) and macrophages. HMGB1-mediated recruitment of leukocytes through the endothelial barrier is linked at least in part to its ability to activate endothelial cells (ECs). The increased expression of various adhesion molecules, at the surface of activated ECs, will in turn stimulates the adhesion of leukocytes, including neutrophils [28-30].In addition, HMGB1 enhances DCs maturation [31,32] and acts in synergy with IL-1, IL-2 and IL-18 to promote interactions between NKs, DCs and monocytes [33,34].
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