The role of innate immune mechanisms in the pathogenesis of localized scleroderma is still not understood. However molecules of innate immunity such as toll-like receptors and cytokines are increasingly seen as a driver for sclerosis development in patients with localized scleroderma. The objective of this study was to investigate the expression of TLR2, HBD-1 and TNF-α genes both in the lesions and unaffected skin areas in patients with localized scleroderma. This study was real time PCR based. It enrolled 63 patients with localized scleroderma including 49 individuals with plaque morphea, 8 individuals with idiopathic atrophoderma of Pasini and Pierini, and 6 individuals with co-occurring plaque morphea and lichen sclerosus. The control group consisted of 8 healthy donors. The study showed the imbalance of innate immune factors in the lesion areas with the reduction in TLR2 gene expression and increase in HBD-1 and TNF-α genes expression compared to healthy donors skin. These changes in the innate immune factors can indicate defects in the processes of pathogene and endogenous ligand recognition, local inflammation development as a result of increased TNF-α expression, and fibroblast activity mediated by a high level of HBD-1 antimicrobial peptide.