Keratin 17 modulates hair follicle cycling in a TN<i>Fα</i>-dependent fashion

The study demonstrated that Keratin 17 (K17) played a crucial role in hair follicle cycling by modulating the transition from anagen to catagen in a TNFα-dependent manner. K17-null mice exhibited alopecia shortly after birth due to hair shaft fragility and premature apoptosis in the hair bulb, indicating an early entry into catagen. The research found that K17-null skin keratinocytes were more sensitive to TNFα, and K17 interacted with TNFR1-associated death domain protein (TRADD), linking K17 to TNFα signaling. Increased NF-κB activity was observed in K17-null skin, and TNFα was necessary for the proper anagen-catagen transition. Ablation of TNFα partially corrected the hair cycling defect in K17-null mice, highlighting K17 and TNFα as key regulators of hair cycling.