Reich Kristian, Hugo Sabine, Middel Peter, Blaschke Volker, Heine Andrea, Gutgesell Carsten, Williams Ruth, Neumann Christine
Department of Dermatology, Georg-August-University, Göttingen, Germany.
J Allergy Clin Immunol. 2002 Apr;109(4):681-7. doi: 10.1067/mai.2002.122234.
The factors controlling infiltration of inflammatory cells into atopic dermatitis (AD) lesions remain to be fully explored. Recently, epidermal cells in lesional AD were reported to contain increased messenger (m)RNA levels of IL-16, a cytokine that induces chemotactic responses in CD4(+)T cells, monocytes, and eosinophils.
We sought to determine the expression of IL-16 in epidermal cells in normal skin and skin from AD lesions and to investigate whether Langerhans cell (LC)-derived IL-16 may contribute to the initiation of atopic eczema.
The cutaneous expression of IL-16 was investigated by in situ hybridization and immunohistochemistry. Expression of IL-16 was also investigated in freshly isolated LCs and in keratinocytes by intracellular cytokine staining, quantitative real-time RT-PCR, and ELISA.
Low levels of IL-16 mRNA, but no stored IL-16 protein, were detected in keratinocytes and LCs isolated from normal skin. Synthesis, storage, and secretion of IL-16 could be induced in LCs, but not keratinocytes, by activation with phorbol ester and ionomycin. In normal skin (n = 10) neither keratinocytes nor LCs expressed IL-16. In contrast, IL-16 was contained in approximately 40% of CD1a(+)LCs in patients with active AD (n = 16). IL-16 expression in LCs in patients with AD correlated with the number of infiltrating CD4(+)cells (r =.72, P =.0017) and was completely downregulated parallel to the clinical response of AD lesions to topical treatment with FK506.
LC-derived IL-16 may participate in the recruitment and activation of inflammatory cells in AD.
控制炎性细胞浸润至特应性皮炎（AD）皮损中的因素仍有待充分探究。最近有报道称，AD皮损中的表皮细胞白细胞介素-16（IL-16）信使核糖核酸（mRNA）水平升高，IL-16是一种可诱导CD4(+)T细胞、单核细胞和嗜酸性粒细胞产生趋化反应的细胞因子。
我们试图确定正常皮肤和AD皮损皮肤中表皮细胞IL-16的表达情况，并研究朗格汉斯细胞（LC）来源的IL-16是否可能参与特应性湿疹的发病。
通过原位杂交和免疫组织化学研究IL-16的皮肤表达情况。还通过细胞内细胞因子染色、定量实时逆转录聚合酶链反应（RT-PCR）和酶联免疫吸附测定（ELISA）研究了新鲜分离的LC和角质形成细胞中IL-16的表达。
从正常皮肤分离的角质形成细胞和LC中检测到低水平的IL-16 mRNA，但未检测到储存的IL-16蛋白。佛波酯和离子霉素激活可诱导LC合成、储存和分泌IL-16，但不能诱导角质形成细胞。在正常皮肤（n = 10）中，角质形成细胞和LC均不表达IL-16。相比之下，活动性AD患者（n = 16）中约40%的CD1a(+)LC含有IL-16。AD患者LC中IL-16的表达与浸润的CD4(+)细胞数量相关（r =.72，P =.0017），并且与AD皮损外用FK506治疗的临床反应平行完全下调。
LC来源的IL-16可能参与AD中炎性细胞的募集和激活。
