Abstract. Disequilibrium of dermal wound repair can result in continued accumulation of ECM and excessive scar formation. In susceptible genetically predisposed individuals, keloid formation can be observed. Keloid disease represents a benign dermal fibroproliferative tumor that is unique to humans. TGF-ß is known to play a key role in the pathogenesis of this disease which is still not fully understood. The isoforms TGF-ß1 and TGF-ß2 have profibrotic properties, whereas TGF-ß3 may have antifibrotic functions. TGF-ß exerts its influence by binding to type I and type II TGF-ß receptors, thereby forming a complex and activating specific downstream effector molecules. The aim of this study was to investigate the effect of TGF-ß1 targeting by antisense oligonucleotides on the RNA synthesis and protein expression of TGF-ß isoforms and their receptors in keloid-derived fibroblasts. In tissue samples with normal fibroblasts (NFs) serving as control samples, expression of TGF-ß1 and -ß2 was decreased when compared to keloid fibroblasts (KFs), while expression of TGF-ß3 and of TGF-ßRII was significantly higher in NFs. In the ELISA assay, abrogation of TGF-ß1 led to a significant decrease in TGF-ß1 and -ß2 (p<0.05). Expression of TGF-ß2 mRNA was reduced. Expression of TGF-ß3 mRNA revealed contrary patterns in KFs from different patients while expression of TGF-ßRI was found to be equal during the measurement period. TGF-ßRII mRNA expression was increased after 48 and 72 h respectively. There is growing evidence for a regulatory mechanism between TGF-ß1 and its receptors. Our findings support this theory by suggesting interrelations between the different TGF-ß isoforms and their receptors. Abnormal response of KFs to TGF-ß might reflect a modification in the regulatory pathway that occurs at the receptor level or during intracellular transduction. Improving the understanding of TGF-ß in keloid disease could lead to the development of clinically useful therapeutic modalities for treatment of keloid disease or even allow identification of preventive strategies.