Technology



(A) Chronic wounds persist in the inflammatory phase through IL-1β- and TNF-α-mediated autocrine recruitment and activation of pro-inflammatory M1 macrophages.

(B) ABCB5+ MSCs, by adaptive release of IL-1RA, break the vicious cycle of autocrine M1 macrophage activation, thus shifting the balance from M1 macrophage-dominated inflammation to M2 macrophage-dominated healing-promoting tissue environment characterized by decreased levels of pro-inflammatory cytokines TNF-α, IL-12 and IL-23, and increased levels of anti-inflammatory cytokine IL-10.

ABCB5+ MSCs trigger switch from pro-inflammatory M1 to anti-inflammatory M2 macrophages





Localized
inflammations

e.g. chronic, non-healing wounds

Generalized
inflammatory processes

e.g. recessive, dystrophic Epidermolysis bullosa

Systemic life-threatening
inflammations

e.g. acute-on-chronic-liver failure

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