背景:光环痣,也被称为萨顿的痣,是被白癜风包围的痣细胞痣,被认为是由T细胞介导的对痣抗原的免疫反应引起的。免疫微环境是神秘的,然而,因为即使去除痣细胞,白癜风通常也不会改善。
目的:分析痣切除术后晕痣患者的临床病程和免疫微环境。
方法:我们收集了54例晕痣患者,并进行了多变量分析和免疫组织化学分析,包括使用PhenoCycler®测定的多重免疫细胞表型分析和空间单细胞分析。
结果:多变量分析显示,只有咨询时是否存在寻常型白癜风与切除后周围白癜风的改善有关。与改良病例相比,非改良病例中痣细胞中程序性死亡配体1的表达明显更高。PhenoCycler®测定揭示,CD107a阳性和CD21阳性细胞在改善的病例中比非改善的病例中更普遍。在改进的情况下,活跃的细胞-细胞相互作用,以CD21阳性细胞为中心,被观察到,而在未改善的情况下,细胞间的相互作用是稀疏的。相反,在未改善的病例中观察到CD8阳性细胞和CD3和CD4阳性细胞的密集浸润.
结论:阐明晕痣的免疫微环境也与黑素瘤相关的白癜风有关,并将有助于我们对肿瘤免疫的理解。
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.
OBJECTIVE: 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.
CONCLUSIONS: Elucidation of the immune microenvironment of halo nevus is also relevant to melanoma-associated vitiligo and will contribute to our understanding of tumor immunity.