Deguchi M, Ohtani H, Sato E, Naito Y, Nagura H, Aiba S, Tagami H
Department of Dermatology, Tohoku University School of Medicine, Sendai, Japan.
Arch Dermatol Res. 2001 Sep;293(9):442-7. doi: 10.1007/s004030100255.
To elucidate the pathogenesis of T cell-mediated inflammatory skin diseases, we examined the exact sites where CD8(+) T cells proliferate, correlating them with the localization of antigen-presenting dendritic cells. We performed CD8/Ki-67 double immunohistochemical staining and single staining for CD1a, CD68, and factor XIIIa on sections of paraffin-embedded tissue samples of inflammatory dermatoses in which T lymphocytes are thought to play a crucial role. The dermatoses were lichen planus (12 samples), acute graft-versus host disease (GVHD) (12 samples), chronic GVHD (10 samples), spongiotic dermatitis (8 samples) and psoriasis (7 samples). Labelling for Ki-67 among CD8(+) T cells was predominantly observed in the subepidermal lymphoid infiltrate, and was scanty in the epidermis. This suggested that proliferation of CD8(+) T cells occurred preferentially in the dermis. The labelling index for Ki-67 among dermal and epidermal CD8(+) cells was quite different among the different diseases studied (P < 0.05). They were rich in the subepidermal portion of the dermis of spongiotic dermatitis, acute GVHD and chronic GVHD, but rare in the dermis of psoriasis and lichen planus. A moderate infiltrate was also observed in lesional epidermis of spongiotic dermatitis, acute GVHD and chronic GVHD, whereas they was almost none in the epidermis of psoriasis and lichen planus. CD1a(+) dermal dendritic cells were densely distributed within the lymphoid infiltrate in the affected dermis of spongiotic dermatitis, psoriasis and lichen planus, whereas they were minimal in GVHD. These dermal dendritic cells are candidates as stimulators on T cells in the dermis. In conclusion, the proliferative status of T cells could be an important clue in the elucidation of the pathophysiology of T cell-mediated inflammatory dermatoses.
为阐明T细胞介导的炎症性皮肤病的发病机制,我们检查了CD8(+) T细胞增殖的确切部位,并将其与抗原呈递树突状细胞的定位相关联。我们对石蜡包埋的炎症性皮肤病组织样本切片进行了CD8/Ki-67双重免疫组织化学染色以及CD1a、CD68和因子XIIIa的单染色,这些炎症性皮肤病中T淋巴细胞被认为起着关键作用。这些皮肤病包括扁平苔藓(12个样本)、急性移植物抗宿主病(GVHD)(12个样本)、慢性GVHD(10个样本)、海绵状皮炎(8个样本)和银屑病(7个样本)。在CD8(+) T细胞中,Ki-67标记主要见于表皮下淋巴浸润,而在表皮中较少。这表明CD8(+) T细胞的增殖优先发生在真皮中。在不同研究疾病中,真皮和表皮CD8(+)细胞中Ki-67的标记指数差异很大(P < 0.05)。它们在海绵状皮炎、急性GVHD和慢性GVHD真皮的表皮下部分丰富,但在银屑病和扁平苔藓的真皮中很少见。在海绵状皮炎、急性GVHD和慢性GVHD的皮损表皮中也观察到中度浸润,而在银屑病和扁平苔藓的表皮中几乎没有。CD1a(+)真皮树突状细胞密集分布在海绵状皮炎、银屑病和扁平苔藓受累真皮的淋巴浸润内,而在GVHD中则很少。这些真皮树突状细胞可能是真皮中T细胞的刺激物。总之,T细胞的增殖状态可能是阐明T细胞介导的炎症性皮肤病病理生理学的重要线索。