Bullous pemphigoid (BP) is the most common autoimmune blistering disease and is linked to IgG recognition of 2 hemidesmosomal antigens, that is, BP230 (BP antigen 1) and BP180 (BP antigen 2, collagen XVII). The association of BP with other systemic diseases, particularly neurocognitive diseases, provides a potential clue in the underlying pathogenesis of BP. The role of
HLA‐DQB1*03:01 binding to the immunogenic portion of BP180 provides a potential mechanism by which exposure to neuronal collagen BP180 may lead to cutaneous disease. In our proposed multi‐hit hypothesis, patients with underlying neuronal disease are exposed to previously sequestered self‐antigen, most importantly BP180. Patients with the
HLA‐DQB1*03:01 allele show an increased T‐cell avidity to several epitopes of BP180, particularly the BP180‐NC16a domain. Thus, they have a genetic susceptibility to developing BP upon exposure to the target antigen. In a patient with dysregulation of Th1/Th2 balance, anergy is lost and T‐cells are subsequently primed resulting in the development of functional autoimmunity against the BP180‐NC16a domain leading to clinically overt disease.
Malignant melanoma arising in OCT is a rare disease with poor prognosis. The current mainstay treatment is surgical. Potential benefits of targeted therapy, immunotherapy, and chemotherapy remain to be determined. A limitation of this study is that these melanomas have only been published in case reports.
Scrotal melanoma is rare, aggressive, and is often caught late in the disease course. The authors encourage dermatologists to educate patients and destigmatize genital lesions to increase the likelihood of earlier detection and better patient outcomes.
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