Fig. 7A–C.

Schematic view of the hypothesis and results is shown. (A) During the in vitro maturation (in the absence of IL-1β), chondrocyte-based constructs accumulate a large amount of cartilaginous matrix (dark gray) and express/release lower amounts of IL-8 and MCP-1 and higher amounts of TGF-β1. (B) When implanted in the cartilage defect, mature grafts respond to IL-1β by losing some of the accumulated cartilage matrix (light gray) and enhancing the expression/release of IL-8 and MCP-1 in a transient manner and of TGF-β1. (C) IL-8 and MCP-1 would attract neutrophils, monocytes, and chondroprogenitors from the surrounding tissues. Although the former cells would induce tissue remodeling, the chondroprogenitors, especially in the presence of elevated concentration of TGF-β1, would contribute to the deposition of extracellular matrix. Taken together, the contribution of the different recruited cell types would improve/accelerate cartilage repair processes (see dashed arrow), and the transient nature of the enhanced release of IL-8 and MCP-1 would not induce chronic inflammation processes.