The state of differentiation of cultured human keratinocytes determines the level of intercellular adhesion molecule-1 (ICAM-1) expression induced by gamma interferon.
The state of differentiation of cultured human keratinocytes determines the level of intercellular adhesion molecule-1 (ICAM-1) expression induced by gamma interferon.
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培养的人角质形成细胞的分化状态决定了γ干扰素诱导的细胞间粘附分子-1（ICAM-1）的表达水平。
DOI：
10.1111/1523-1747.ep12499938
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Norris,DA
中科院分区：
文献类型：
--
作者：
Kashihara-Sawami,M;Norris,DA
诱导表皮角质形成细胞表面ICAM-1(CD54)的表达是启动白细胞与表皮相互作用的重要步骤。我们研究了角质形成细胞分化和治疗表皮炎症的药物对这种重要的黏附分子诱导的影响。免疫荧光和流式细胞仪分析细胞间黏附分子-1的表达与角质形成细胞分化的标志物相关。细胞表面细胞间黏附分子-I的表达在所有培养条件下均被7-干扰素诱导，但在低钙(0.03 mM)培养的细胞表面ICAM-1的表达显著增加(p<；0.014)，并与基础细胞角蛋白K5的染色增加相关。合成维甲酸(Ro 10670)在较宽的浓度范围内(10-8~10-5M)增强干扰素诱导的细胞间黏附分子-1的表达，但这种作用仅见于生长在0.15 mM和1.0 mM钙离子中的分化程度较高的细胞，而不存在于生长在0.03 mM钙离子中的细胞。Etretin对细胞内K5染色的影响与对细胞表面ICAM-1的影响相似，抗炎糖皮质激素对培养的人角质形成细胞ICAM-1的表达没有影响，即使在次适的γ干扰素剂量(5U/ml)下也是如此。另一方面，β-雌二醇模拟Etretin效应，在0.15和1.0nM钙离子中增加干扰素诱导分化的角质形成细胞ICAM-1表达和K5染色，而在0.03 mM钙离子中不增加。Etretin和β-雌二醇都减少了终末分化的标志物--总蛋白的染色，支持这样的命题：在这个实验系统中，这些药物抑制角质形成细胞的分化。在基本分化水平的角质形成细胞中，增强的ICAM-1诱导与干扰素对ICAM-1的体内效应相关，并可能是炎症性皮肤病中出现的ICAM-1模式的主要决定因素。
Inducing the expression of ICAM-1(CD54) on the surface of epidermal keratinocytes is an important step, in initiating leukocyte interaction with the epidermis. We studied tile effect of keratinocyte differentiation and of drugs used to treat epidermal inflammation on the induction of this important adhesion molecule. Cell membrane expression of ICAM-1 in cultured human keratinocytes was analyzed using both immunofluorescence and FACS analysis of staining with anti-ICAM-1 monoclonal antibody and was correlated with markers of keratinocyte differentiation.Cell-surface ICAM-I expression was induced by 7 interferon in all culture conditions, but was significantly greater (p < 0.014) in cells grown in low-calcium medium ([Ca++]) 0.03 mM), and correlated with increased staining for the basal cell keratin K5. The synthetic retinoid Etretin (Ro 10670) enhanced the interferon-induced ICAM-1 expression over a wide concentration range (10-8-10-5M); however, this effect was only seen in the more differentiated cells grown in 0.15 mM and 1.0 mM calcium and not in the cells grown in 0.03 mM calcium. The Etretin effects on intracellular K5 staining paralleled those on cell-surface ICAM-1.Anti-inflammatory glucocorticoids had no effect on ICAM-1 expression in cultured human keratinocytes, even at suboptimal γ interferon doses (5 U/ml). β-estradiol, on the other hand, mimicked the Etretin effect, increasing both IFN induction of ICAM-1 expression and K5 staining in more differentiated keratinocytes in 0.15 and 1.0 nM calcium, but not in those in 0.03 mM calcium. Both Etretin and β-estradiol decreased staining of involucrin, a marker of terminal differentiation, supporting the proposition that in this experimental system these drugs suppress keratinocyte differentiation.The enhanced ICAM-1 induction in keratinocytes with a basal level of differentiation correlates with the in vivo effects of interferon on ICAM-1 and may be a principal determinant in the patterns of ICAM-1 seen in inflammatory skin diseases.