Smith K J, Skelton H G, Yeager J, Baxter D, Nelson A T, Angritt P, Chu W, Wagner K F
National Naval Medical Center, Bethesda, Maryland, USA.
J Cutan Med Surg. 1998 Apr;2(4):212-9. doi: 10.1177/120347549800200407.
One important factor in understanding the pathogenesis of human immune deficiency virus (HIV) disease is documenting the patterns of immune dysregulation present in HIV-positive patients. The cells which home to skin are mainly certain subsets of T cells and, as opposed to the peripheral blood, where circulating factors may inhibit terminal phenotypic differentiation, the cutaneous environment potentiates differentiation during cutaneous eruptions.
The authors' aim was to characterize the inflammatory dermatoses in biopsy specimens from HIV-positive patients with immunohistochemical stains for lymphoid markers, activation markers, and adhesion molecules and to determine if there was any correlation with the type of dermatosis and the HIV-disease stage.
Lymphoid and activation markers as well as adhesion molecules were studied on cutaneous biopsy specimens from 96 inflammatory dermatoses in HIV-positive patients. The dermatoses included psoriasiform dermatoses with and without a lichenoid component, perivascular lymphoid dermatoses, perivascular and periadnexal inflammatory dermatoses, spongiotic dermatoses, granulomatous dermatoses, and neutrophilic dermatoses with and without vasculitis.
Although there was a decrease in CD4/CD8 ratios in the cutaneous inflammatory dermatoses with progression of the disease, the ratios of CD4/CD8 cells were far higher than those in the peripheral blood. There were also increasing numbers of CD23+ cells and increased E-Selectin expression on endothelial cells from the early stages of disease, with no consistent pattern of ICAM-1 expression on epithelial cells with disease progression.
The expression of lymphoid markers, activation markers, and adhesion molecules in the skin with progression of HIV disease, is consistent with a T helper (Th)1 to Th0/Th2 cytokine pattern of immune dysregulation. This cytokine pattern may be modified by the cytopathic effects of HIV on lymphoid and dendritic populations and by effects of other concurrent infections. Significant numbers of CD4+ T cells in skin infiltrates, with low peripheral CD4 T-cell counts, suggest that the cutaneous T-cell populations may be distinctive.
了解人类免疫缺陷病毒（HIV）疾病发病机制的一个重要因素是记录HIV阳性患者中存在的免疫失调模式。归巢至皮肤的细胞主要是某些T细胞亚群，与外周血不同，在外周血中循环因子可能抑制终末表型分化，而皮肤环境在皮肤发疹期间会促进分化。
作者旨在通过对HIV阳性患者活检标本进行免疫组化染色，检测淋巴标记物、活化标记物和黏附分子，以对炎症性皮肤病进行特征性描述，并确定其与皮肤病类型和HIV疾病分期是否存在相关性。
对96例HIV阳性患者的炎症性皮肤病皮肤活检标本进行淋巴标记物、活化标记物及黏附分子研究。这些皮肤病包括有或无苔藓样成分的银屑病样皮肤病、血管周围淋巴性皮肤病、血管周围及腺周炎性皮肤病、海绵状皮肤病、肉芽肿性皮肤病以及有或无血管炎的嗜中性皮肤病。
尽管随着疾病进展，皮肤炎症性皮肤病中的CD4/CD8比值下降，但CD4/CD8细胞比值远高于外周血中的比值。从疾病早期开始，CD23+细胞数量也在增加，内皮细胞上的E选择素表达增加，随着疾病进展，上皮细胞上的细胞间黏附分子-1（ICAM-1）表达无一致模式。
随着HIV疾病进展，皮肤中淋巴标记物、活化标记物和黏附分子的表达与免疫失调的T辅助（Th）1向Th0/Th2细胞因子模式一致。这种细胞因子模式可能会因HIV对淋巴和树突状细胞群体的细胞病变作用以及其他并发感染的影响而改变。皮肤浸润中有大量CD4+T细胞，而外周血CD4 T细胞计数较低，这表明皮肤T细胞群体可能具有独特性。
