Abstract
In the pathogenesis of keloids, the immune response seems to be of great
importance. In the normal wound healing process, interferon (IFN)-a downregulates
collagen synthesis (26,53), IFN-g reduces collagenase activity (53), and IFN-a, -b,
and -g inhibit keloidal fibroblast production of collagen I, III, and VI and reduce
messenger RNA proliferation of rapidly dividing fibroblasts (51). Reductions of
IFN-a, IFN-g, and tumor necrosis factor-a concentration have been found in keloids
(22,31,52). IFN-a and -b also reduce fibroblast production of glycosaminoglycans
(GAGs), which form the scaf-folding for deposition of dermal collagen. IFN-g
enhances GAG production (53). Studies have shown that IFN-g modulates a p53
apoptotic pathway by inducing apoptosis-related genes.