However, excessive activation of TLR2 or TLR4 in dFBs by endogenous DAMPs such as TLR4 ligands hyaluronan, fibrinogen, and other ECM proteins or TLR2 ligand serum amyloid A (SAA) may lead to the pathogenesis of fibrotic skin disorders, such as hypertrophic scarring and systemic sclerosis (SSc) [43–45]. Here, TLR4 is linked to systemic sclerosis.