Similarly, in a model of crescentic glomerulonephritis, TGF-β1 overexpression leads to a 70% decrease in the accumulation of T cells and macrophages and reduced expression of renal IL-1β, TNF-α, and MCP-1 by 70 to 80% in comparison to wild-type animals [15]. In vitro study, performed on human kidney tubular epithelial cells (HKC-8), showed that one of the possible mechanisms of anti-inflammatory effect of TGF-β1 relies on the inhibition of RANTES expression through β-catenin-triggered blockade of NF-κB signaling [20]. Here, TGFB1 is linked to crescentic glomerulonephritis.