Burrows N P, Molina F A, Terenghi G, Clark P K, Haskard D O, Polak J M, Jones R R
Department of Histochemistry, Royal Postgraduate Medical School, Hammersmith Hospital, London.
J Clin Pathol. 1994 Oct;47(10):939-44. doi: 10.1136/jcp.47.10.939.
To compare the expression of the cell adhesion molecules intercellular adhesion molecule-1 (ICAM-1), ELAM-1 (E-selectin), and vascular cell adhesion molecule-1 (VCAM-1) in cutaneous leucocytoclastic and lymphocytic vasculitis.
Immunohistochemical analysis was performed on early lesional skin biopsy specimens of leucocytoclastic vasculitis (n = 14), lymphocytic vasculitis (n = 10), non-lesional skin (n = 12), and normal skin (n = 5). A standard immunoperoxidase technique was used to detect expression of ICAM-1, E-selectin, VCAM-1, and the cell markers CD11a, CD11b, CD11c, von Willebrand factor, CD3, CD68, and neutrophil elastase (NP57).
Basal keratinocyte intercellular adhesion molecule-1 was expressed in eight (80%) cases of lymphocytic and in only one (7%) case of leucocytoclastic vasculitis, and not in non-lesional skin or control biopsy specimens from normal subjects. E-selectin was expressed on vascular endothelium in eight (57%) cases of leucocytoclastic and in seven (70%) cases of lymphocytic vasculitis. Endothelial vascular cell adhesion molecule-1 expression was seen in three (21%) biopsy specimens of leucocytoclastic and five (50%) of lymphocytic vasculitis. There were increased numbers of cells in the dermal infiltrate stained for NP57, CD11b, and CD11c in leucocytoclastic compared with lymphocytic vasculitis (p < 0.001, p = 0.013, p = 0.009, respectively); immunoreactive positive cells for CD3 and CD11a were increased in lymphocytic compared with leucocytoclastic vasculitis (p < 0.001, p = 0.011, respectively).
These observations indicate that upregulation of adhesion molecule expression occurs in both leucocytoclastic and lymphocytic vasculitis. The different patterns of adhesion molecule expression in the two groups of vasculitis may reflect differences in the local release of cytokines. In particular, detection of intercellular adhesion molecule-1 expression by keratinocytes in lymphocytic vasculitis is consistent with an active role for mediators derived from T lymphocytes in the pathogenesis of the lesion.
比较细胞间黏附分子-1（ICAM-1）、ELAM-1（E-选择素）和血管细胞黏附分子-1（VCAM-1）在皮肤白细胞破碎性血管炎和淋巴细胞性血管炎中的表达。
对白细胞破碎性血管炎（n = 14）、淋巴细胞性血管炎（n = 10）、非病变皮肤（n = 12）和正常皮肤（n = 5）的早期病变皮肤活检标本进行免疫组织化学分析。采用标准免疫过氧化物酶技术检测ICAM-1、E-选择素、VCAM-1以及细胞标志物CD11a、CD11b、CD11c、血管性血友病因子、CD3、CD68和中性粒细胞弹性蛋白酶（NP57）的表达。
基底角质形成细胞间黏附分子-1在8例（80%）淋巴细胞性血管炎病例中表达，而在白细胞破碎性血管炎病例中仅1例（7%）表达，在非病变皮肤或正常受试者的对照活检标本中未表达。E-选择素在8例（57%）白细胞破碎性血管炎和7例（70%）淋巴细胞性血管炎病例的血管内皮细胞上表达。内皮血管细胞黏附分子-1表达见于3例（21%）白细胞破碎性血管炎活检标本和5例（50%）淋巴细胞性血管炎活检标本。与淋巴细胞性血管炎相比，白细胞破碎性血管炎中真皮浸润内NP57、CD11b和CD11c染色的细胞数量增加（分别为p < 0.001、p = 0.013、p = 0.009）；与白细胞破碎性血管炎相比，淋巴细胞性血管炎中CD3和CD11a免疫反应阳性细胞增加（分别为p < 0.001、p = 0.011）。
这些观察结果表明，白细胞破碎性血管炎和淋巴细胞性血管炎中均出现黏附分子表达上调。两组血管炎中黏附分子表达的不同模式可能反映细胞因子局部释放的差异。特别是，淋巴细胞性血管炎中角质形成细胞间黏附分子-1表达的检测与T淋巴细胞衍生的介质在病变发病机制中的积极作用一致。
