Our study underscores cases of Middle Eastern MDM with SLURP1 mutations and skin malignancies at PPK sites. Our findings also highlight a plausible epithelial lineage-specific tumor suppressor role for the SLURP1 gene, as well as a role in the development and metastasis of melanoma and thus a potential molecular signature for melanoma.

pDCs constitute a central component of the inflammatory infiltrate in PL, suggesting that PL shares with the other entities that exhibit an ID a common pDC-driven process through type I IFN production, which ultimately leads to the cytotoxic attack.

Lichen striatus (LS) is an unusual, acquired, self-limiting, cutaneous disorder that commonly presents as unilateral, linearly arranged erythematous papules along the lines of Blaschko on the neck, trunk or limbs, which usually presents in children but it may be seen in adults. 1 After an abrupt appearance, LS lesions usually involute in 1-2 years. The aetiology of LS is unclear. 1 Suggested contributing factors include autoimmune response, atopy, genetic predisposition, viral infection and vaccination. Among the latter, LS has been reported to occur in patients after receipt of bacille Calmette-Gu erin (BCG), hepatitis B virus (HBV), and measles, mumps and rubella (MMR) vaccinations. 2-4 We describe a 32-year-old woman whose LS developed after yellow fever vaccination, an association that has not been reported previously.A 32-year-old woman from Ghana presented with a 3-month history of occasionally pruritic lesions on her left arm and hand. She was previously healthy, and her medical history was unremarkable, except for yellow fever vaccination 6 weeks prior to the onset of the skin lesions. The lesions had started at the site of the vaccine injection on the upper arm and extended down the arm and later involved the hand.On examination, the patient was found to have linear streaks of hypopigmented, flat-topped, slightly raised, scaly papules on the left arm and hand (Fig. 1a,b). There were no lesions elsewhere.Histopathology showed hyperkeratosis and a lichenoid interface dermatitis with dense band-like and perieccrine lymphocytic infiltrates (Fig. 1c,d).These findings were consistent with LS. Clobetazol propionate cream once daily was prescribed, which resulted in clearance of the lesions in 4 weeks with residual postinflammatory hyperpigmentation.Yellow fever is a potentially fatal, mosquito-borne, infectious viral disease endemic to areas of South America and Africa. 5 The yellow fever vaccine is considered one of the safest and most effective vaccines, and is recommended to those travelling to high-risk areas. It is a live attenuated version of the 17D strain grown in egg embryos, and imparts durable immunity for 10 years. (a) (b) (c) (d) Figure 1 (a,b) Linear streaks of hypopigmented, flat-topped, slightly elevated scaly papules on patient's left arm and hand. (c,d) Hyperkeratosis and lichenoid interface dermatitis with dense band-like and perieccrine lymphocytic infiltrates. Haematoxylin and eosin, original magnification: (c) 9 40; (d) 9 200.

Plasmacytoid dendritic cells (pDCs) are the most potent producers of type I interferons (IFNs), which allows them to provide anti-viral resistance and to link the innate and adaptive immunity by controlling the function of myeloid DCs, lymphocytes, and natural killer cells. pDCs are involved in the pathogenesis of several infectious [especially viral, such as Molluscum contagiosum (MC)], inflammatory/autoimmune, and neoplastic entities. Kaposi's sarcoma (KS) is a multifocal, systemic lympho-angioproliferative tumor associated with Kaposi's sarcoma-associated herpesvirus (KSHV) infection. Microscopy typically exhibits a chronic inflammatory lymphoplasmacytic infiltrate in addition to the vascular changes and spindle cell proliferation. Despite the extensive research done on the immune evasion strategies employed by KSHV, pDCs role in relation to KS has only rarely been investigated. Given this, we intend to investigate pDC occurrence and activity in the skin lesions of KS. Immunohistochemical staining for BDCA-2 (specific pDC marker) and MxA (surrogate marker for local type I IFN production) was performed on classic KS (n = 20) with the control group comprising inflamed MC (n = 20). As expected, BDCA-2+ pDCs were present in abundance with diffuse and intense MxA expression (indicative of local type I IFN production) in all inflamed MC cases (20 of 20, 100 %). Though present in all the KS cases, pDCs were significantly less abundant in KS than in inflamed MC cases, and MxA expression was patchy/weak in most KS cases. In summary, pDCs are part of the inflammatory host response in KS; however, they were generally low in number with decreased type I IFN production which is probably related to KSHV's ability to evade the immune system through the production of different viral proteins capable of suppressing IFN production as well as pDC function.

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