Ohki O, Yokozeki H, Katayama I, Umeda T, Azuma M, Okumura K, Nishioka K
Department of Dermatology, Tokyo Medical and Dental University School of Medicine, Japan.
Br J Dermatol. 1997 Jun;136(6):838-45.
Recently, we reported the functional expression of CD86 on cultured human Langerhans cells derived from normal epidermis. In the present study, we investigated the expression and function of co-stimulatory molecules in the pathogenesis of atopic dermatitis. In immunohistochemical analysis, CD80 and/or CD86 were detected on dendritic-shaped cells not only in the epidermis but also in the dermis in the inflammatory lesions of atopic dermatitis (n = 12). CD80 was expressed in only five cases (42%), while CD86 was expressed in all cases (100%). These molecules were not detected in normal control subjects (n = 8). In non-lesional skin of atopic dermatitis (n = 4), CD86 but not CD80 was detected in one case. CD86 was preferentially induced on dendritic-shaped cells in positive patch test sites to Dermatophagoides pteronyssinus or house dust allergen in atopic dermatitis (n = 4). The CD80- or CD86-positive cells were confirmed as Langerhans cells by double immunostaining using anti-CD1a monoclonal antibody. Neither CD86 nor CD80 was detected on keratinocytes. Similar results of the stronger expression of CD86 over that of CD80 were obtained from psoriasis vulgaris (n = 11) and from contact dermatitis (n = 7), although CD86 was expressed only in 57% of the contact dermatitis cases. The percentage of Langerhans cells positive for CD86 was higher than for CD80, i.e. 48% compared with 9%, respectively, in the epidermis of lesional skin of atopic dermatitis (n = 8). The expression rate of these molecules on Langerhans cells increased in the dermis. To investigate the function of co-stimulatory molecules on Langerhans cells in atopic dermatitis, we conducted an inhibition test with antibodies. Anti-CD86 monoclonal antibody almost completely inhibited T-cell proliferation stimulated with crude extract of D. pteronyssinus in the presence of epidermal cells as antigen-presenting cells, whereas anti-CD80 monoclonal antibody produced less of an inhibitory effect. These data indicate that CD86 expressed on Langerhans cells may play an important part in the pathogenesis of atopic dermatitis.
最近，我们报道了从正常表皮分离培养的人朗格汉斯细胞上CD86的功能性表达。在本研究中，我们调查了共刺激分子在特应性皮炎发病机制中的表达及功能。免疫组织化学分析显示，在特应性皮炎炎性皮损（n = 12）的表皮及真皮中，树突状细胞上可检测到CD80和/或CD86。仅5例（42%）表达CD80，而所有病例（100%）均表达CD86。正常对照者（n = 8）未检测到这些分子。在特应性皮炎的非皮损皮肤（n = 4）中，1例检测到CD86而未检测到CD80。在特应性皮炎患者对粉尘螨或屋尘变应原的阳性斑贴试验部位，树突状细胞上优先诱导表达CD86（n = 4）。使用抗CD1a单克隆抗体进行双重免疫染色，证实CD80或CD86阳性细胞为朗格汉斯细胞。角质形成细胞上未检测到CD86和CD80。寻常型银屑病（n = 11）和接触性皮炎（n = 7）也得到了类似结果，即CD86表达强于CD80，尽管接触性皮炎病例中仅57%表达CD86。在特应性皮炎皮损皮肤（n = 8）的表皮中，CD86阳性的朗格汉斯细胞百分比高于CD80阳性的朗格汉斯细胞，分别为48%和9%。这些分子在真皮中朗格汉斯细胞上的表达率更高。为研究特应性皮炎中朗格汉斯细胞上共刺激分子的功能，我们用抗体进行了抑制试验。抗CD86单克隆抗体在存在表皮细胞作为抗原呈递细胞的情况下，几乎完全抑制了粉尘螨粗提物刺激的T细胞增殖，而抗CD80单克隆抗体的抑制作用较小。这些数据表明，朗格汉斯细胞上表达的CD86可能在特应性皮炎发病机制中起重要作用。
