Background: Halo nevus, also called Sutton's nevus, is a nevus cell nevus surrounded by vitiligo thought to be caused by a T-cell mediated immune response to the nevus antigen. The immune microenvironment is mysterious, however, as vitiligo often does not improve even when the nevus cells are removed.
Objectives: To analyze the clinical course and immune microenvironment of patients with halo nevus who had undergone nevus excision.
Methods: We collected 54 halo nevus patients and performed multivariate analysis and immunohistochemical analysis, including multiplexed immune cell phenotyping and spatial single-cell analyses using the PhenoCycler® assay.
Results: Multivariate analysis revealed that only the presence or absence of vitiligo vulgaris at the time of consultation was associated with improvement in the surrounding vitiligo following excision. Expression of programmed death-ligand 1 in nevus cells was significantly higher in non-improved cases compared with improved cases. The PhenoCycler® assay revealed that CD107a-positive and CD21-positive cells were more prevalent in improved cases than in non-improved cases. In the improved cases, active cell-cell interactions, centered on CD21-positive cells, were observed, whereas in the non-improved cases, cell-cell interactions were sparse. Instead, a dense infiltration of CD8-positive cells and CD3 and CD4-positive cells was observed in non-improved cases.
Conclusion: Elucidation of the immune microenvironment of halo nevus is also relevant to melanoma-associated vitiligo and will contribute to our understanding of tumor immunity.
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http://dx.doi.org/10.1016/j.jdermsci.2023.03.004 | DOI Listing |
J Med Case Rep
January 2025
Department of Dermatology and Venereology, Faculty of Medicine, University of Aleppo, Aleppo, Syria.
Background: Basal cell nevus syndrome, also known as Gorlin or Gorlin-Goltz syndrome, is a hereditary condition caused by mutation in the PATCHED gene. The syndrome presents with a wide range of clinical manifestations, including basal cell carcinomas, jaw cysts, and skeletal anomalies. Diagnosis is based on specific criteria, and treatment typically includes surgical removal of basal cell carcinomas.
View Article and Find Full Text PDFPlast Reconstr Surg Glob Open
January 2025
From the Division of Plastic and Reconstructive Surgery, Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon.
Giant congenital melanocytic nevi are large pigmented premalignant lesions present at birth that have an associated risk of malignant transformation. Full-thickness excision of these lesions would be required to eliminate this risk. However, giant nevi can leave behind large defects that can be challenging to reconstruct.
View Article and Find Full Text PDFAustralas J Dermatol
January 2025
QCIF Bioinformatics, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland, Australia.
Background/objectives: Congenital melanocytic naevi (CMN) are a risk factor for melanoma. Melanoma risk is dependent on the congenital phenotype. Our primary aims were to assess the clinical characteristics of CMN that indicate a high risk of neurocutaneous melanosis (NCM) and melanoma in an Australian paediatric population group; to identify patient characteristics and clinical features of CMN that trigger further investigations; and to determine the rate of malignancy and other complications for CMN.
View Article and Find Full Text PDFBMJ Case Rep
January 2025
Dermatology, Zuckerberg San Francisco General Hospital, University of California San Francisco, San Francisco, California, USA.
A woman in her 70s with well-controlled HIV on antiretroviral therapy presented with a several-month history of an asymptomatic perianal lesion. Skin examination showed a 0.5-1 cm red-pink, shiny, exophytic papule with visible telangiectasias near the anal verge.
View Article and Find Full Text PDFCureus
January 2025
College of Dentistry, King Saud University, Riyadh, SAU.
Oral melanocytic nevi (OMN) are rare benign tumors originating from melanocytes with an unclear pathogenesis. The current theory suggests that OMN originate from dormant dendritic melanocytes that become enclosed in the dermis during the embryonic migration of melanoblasts - the precursors of melanocytes - from the neural crest to the epidermis. OMN can be congenital or acquired, with acquired nevi being more common.
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