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The study on lichen planopilaris (LPP) involved 42 adult patients and demonstrated that the disease was characterized by the collapse of immune privilege in the hair follicle's epithelial stem cell niche, specifically in the bulge area. This collapse was marked by increased expression of MHC class I and II molecules and a reduction in TGFβ2 and CD200 expression, leading to a Th1-biased cytotoxic T cell response. The findings suggested that interferon-γ (IFNγ) played a significant role in this process, indicating that LPP might be an autoimmune disease. The study proposed that protecting or restoring immune privilege in the bulge could be a therapeutic strategy for managing this form of cicatricial alopecia.

The document reviewed the role of the hedgehog (Hh) signalling pathway in skin development and cancer, particularly basal cell carcinoma (BCC), which affected 750,000 Americans annually. It highlighted how mutations in genes like PATCHED (PTCH), sonic hedgehog (Shh), and smoothened (Smo) expanded the understanding of BCC's genetic basis. The Shh pathway was crucial for stem cell maintenance and hair follicle and sebaceous gland development in the skin, though it played a minimal role in adult tissues. The review summarized studies on the Shh pathway's involvement in skin development and cancer, described animal models based on this pathway, and discussed chemoprevention strategies for BCCs, providing insights into molecular target-based prevention and treatment of skin cancer.

The study demonstrated that the loss of Patched 1 (Ptch1) function in the basal cell population of mouse skin was sufficient to induce rapid skin tumor formation, similar to human basal cell carcinoma (BCC). The research showed that Ptch1 did not affect the nuclear translocation of β-catenin or activate the Notch pathway, but its absence led to the nuclear accumulation of cell cycle regulators cyclin D1 and B1. This suggested that Ptch1 acted as a tumor suppressor by inhibiting cell cycle progression at the G1-S and G2-M phases, functioning as a "gatekeeper." The mouse model used in this study, due to its high frequency and rapid onset of tumors, was considered ideal for testing therapeutic strategies, including Patched pathway inhibitors.

The study revealed that the opioid system, particularly through delta opioid receptors (DOR), played a significant role in regulating cutaneous mechanosensation, including both touch and pain. DORs were found on myelinated mechanoreceptors associated with structures like Meissner corpuscles and Merkel cell-neurite complexes. These receptors also appeared on a subset of nociceptors coexpressing mu and delta opioid receptors. Activation of DORs at the central terminals of these mechanoreceptors inhibited synaptic input to the spinal dorsal horn by blocking voltage-gated calcium channels. This mechanism suggested that targeting DOR could be a potential strategy for managing injury-induced mechanical hypersensitivity.