KRT15 and cicatricial alopecia: Clinically, this may be relevant for irreversible forms of human hair loss characterized by a loss of K15+/CD200+ bulge cells and a collapse of the HF bulge immune privilege [91], like the cicatricial alopecia, lichen planopilaris [61], where insufficient ß1 integrin-mediated signaling may contribute to the CD200-dependent component of the HF bulge immune privilege collapse demonstrated in this scarring hair loss disorder [91].