033 Excision of halo nevus without PD-L1 expression may cure vitiligo

Abstract

Halo nevus (HN), also called Sutton nevus, is a nevus cell nevus that is surrounded by vitiligo and is caused by a T-cell mediated immune response to the nevus antigen. Excision of nevus is recommended to prevent progression to vitiligo vulgaris. When vitiligo may occur around malignant melanoma, hemangioma, blue nevus, neurofibroma, senile wart, etc, it’s called Sutton’s phenomenon. Especially, vitiligo in melanoma patients is called “melanoma-associated vitiligo” and recognized to associate with favorable outcomes. It’s sometimes observed in patients who respond to immune checkpoint inhibitor (ICI) therapy as a “preferable” immune-related adverse event (irAE), the mechanism has attracted attention. However, there are few reports on analyses of immune checkpoint including PD-1/PD-L1 in HN. In the present study, to evaluate the relationship between immune checkpoint including PD-1/PD-L1 and HN, we performed immunohistochemical analysis using formalin-fixed paraffin-embedded (FFPE) samples collected from 38 HN patients (16 males and 22 females, mean age 20.47 years) whose nevus were resected in Nagoya City University Hospital. Of the 29 cases that we were able to follow after nevus excision, 12 cases showed improvement of the surrounding vitiligo and 17 cases showed no change or expansion of vitiligo. 25 cases have vitiligo vulgaris, and 10 of them showed improvement of vitiligo vulgaris after HN excision. Immunohistochemical findings showed that PD-L1 expression was positive in 25 of 36 cases, and cases with improved vitiligo after nevus excision were predominantly PD-L1 negative. PD-1 expression in infiltrating cells was positive in 19 of 38 patients, but there was no significant correlation between PD-1 expression and improvement of vitiligo. These results suggest that more than local immune responses are involved in vitiligo formation in PD-L1-positive HN, and the analysis of immune responses in PD-L1-positive HN may lead to elucidation of the mechanisms of tumor immunity and irAEs