後天性の色素性母斑は,組織学的には境界母斑に端を発し,真皮内へ増殖する.その細胞形態と配列は表皮から真皮深層まで段階的な移行を示し,真皮深層ではメラニンを欠き,線維化やneuroid transitionをきたす.これらの変化は経年的に発現し,隆起の増加,平坦化や色調の変化などの臨床所見とも相関する.近年,免疫組織化学的染色法の発展に伴い,メラノサイト系腫瘍について多くの検討がなされてきた.悪性腫瘍の鑑別診断を目的とした研究に比較して,良性の後天性色素性母斑の発生や増殖機転に関する研究は少ない.本研究では,色素性母斑における細胞分裂とアポトーシスの関係を明らかにすることを目的とした.後天性の色素性母斑のうち,HE染色で真皮浅層で胞巣形成,深層にneuroid componentを認めた15例(真皮内母斑10例,複合母斑5例)に対し,抗S-100抗体,抗Bcl-2抗体,抗Bax抗体,抗Ki-67抗体およびTUNEL法で免疫組織化学的染色を行った.母斑細胞数100当りの各マーカー陽性細胞数を,真皮内胞巣形成部位と真皮深部のneuroid componentとで比較し,また,各マーカー間の相関関係について検討した.S-100,Bcl-2およびTUNEL法では全例に陽性細胞がみられたが,Baxでは全例が陰性であった.Bcl-2では胞巣部分で有意に陽性細胞数が多かったのに対し,TUNEL法ではneuroid componentで有意に陽性細胞数が優勢であった.MIB-1は双方で少数の陽性反応を示したが,有意差は明らかでなかった.各マーカー陽性細胞は,両部位間で相関を示したが,各マーカー間での相関はみられなかった.この結果より,母斑細胞は真皮内に増殖していく過程で一定の細胞分裂能を保つと考えられた.また,真皮浅層ではアポトーシス抑制を受けているが,真皮深層ではアポトーシス細胞は増加しており,アポトーシス抑制の喪失により細胞数が制御されていることが推測された.Benign melanocytic nevi have histological characteristics in clinical growth. Individual cells are derived from dermoepidermal junction and disperse into deeper part of the dermis with secondary changes. The aim of this study is to compare proliferative activity and apoptotic behavior of nevus cells in its \u27life cycle\u27. Acquired nevi (10 intradermal nevi and 5 compound nevi) of 15 patients were immunostained using anti S-100 antibody, anti Bcl-2 antibody, anti Bax antibody, anti-Ki-67 (MIB-1) antibody and by terminal deoxynucleotidyl-transferase mediated nick end labelling (TUNEL) method. Cell populations of reaction positive cells were compared between intradermal nest-forming lesions of the superficial part of the dermis and neurotized lesions of the deeper part. Correlations between markers regarding immunostaining characteristics of various cells were also examined. Both parametric and non-parametric methods (t-test and Wilcoxon\u27s signed-rank test) were used for statistical analysis. S-100, Bcl-2 and TUNEL positive cells were recognized in all cases, while no section was stained with Bax. According to Bcl-2, population of positively-stained cells in the nest-forming lesions was significantly larger than in neurotized lesions by 5 cells (per one hundred S-100 positive cells). As to TUNEL, neurotized lesion had nearly 9 more TUNEL-positive cells (per one hundred S-100 positive cells) as oppose to the other lesion. Mean difference of MIB-1 positive cell population between the two lesions was 0.08 (p=0.012). Also, correlations were significant between expressions in the two lesions for each same marker while there were no significant correlations between the three markers. In conclusion, this study suggests that nevus cells keep some proliferating ability in most location through entire life of nevi as confirmed by MIB-1 expression. Increased cells did not tend to go into apoptosis in the superficial part, where newly proliferated cells compiled in the early part of life cycle, ensured by Bcl-2 expression while nevoid cells dispersed down into deeper part of the dermis seem to lose the Bcl-2 expression and to increase TUNEL positive expression. The protection against apoptosis may become a dominant factor in regulating the cell numbers compared to proliferation in benign melanocytic nevi
