Gene expression based evidence of innate immune response activation in the epithelium with oral lichen planus.

Gene expression based evidence of innate immune response activation in the epithelium with oral lichen planus.
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DOI:
10.1016/j.archoralbio.2013.12.010
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发表时间:
2014-03
影响因子:
3
通讯作者:
Schwartz JL
Schwartz JL
中科院分区:
医学4区
文献类型:
--
作者:
Adami GR;Yeung AC;Stucki G;Kolokythas A;Sroussi HY;Cabay RJ;Kuzin I;Schwartz JL

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口腔扁平苔藓(Oral lichen planus,OLP)是一种原因不明的口腔粘膜疾病,其病变伴随着T细胞向上皮下的强烈带状炎性浸润和角质形成细胞的死亡。为了更好地了解角质形成细胞在这些疾病中的作用,我们对OLP及其姐妹疾病口腔苔藓样反应(OLR)受试者的口腔上皮病变进行了基因表达分析。14名OLP或OLR患者被纳入研究,沿着的是23名患有各种口腔疾病的受试者的对照组和17名没有临床可见的粘膜异常的受试者的正常组。基于在由上皮、基质和免疫细胞组成的组织样品中检测到分泌蛋白或RNA水平的变化,各种蛋白质已与OLP相关。在三组中检测了在上皮中表达的这些基因中的12个的mRNA水平。四个基因在OLP患者的上皮中表现出增加的表达:CD14、CXCL1、IL8和TLR1,并且这些蛋白质中的至少两个,TLR1和CXCL1,在口腔角质形成细胞中以实质水平表达。由于T细胞在OLP病变中的大量积累,长期以来一直认为这是一种适应性免疫功能障碍。我们提供的证据表明,有先天免疫基因在上皮细胞与这种疾病的表达增加,这表明在疾病和一个可能的治疗目标,这一过程中的作用。
Oral lichen planus (OLP) is a disease of the oral mucosa of unknown cause producing lesions with an intense band-like inflammatory infiltrate of T cells to the subepithelium and keratinocyte cell death. We performed gene expression analysis of the oral epithelium of lesions in subjects with OLP and its sister disease, oral lichenoid reaction (OLR), in order to better understand the role of the keratinocytes in these diseases. Fourteen patients with OLP or OLR were included in the study, along with a control group of 23 subjects with a variety of oral diseases and a normal group of 17 subjects with no clinically visible mucosal abnormalities. Various proteins have been associated with OLP, based on detection of secreted proteins or changes in RNA levels in tissue samples consisting of epithelium, stroma, and immune cells. The mRNA level of twelve of these genes expressed in the epithelium was tested in the three groups. Four genes showed increased expression in the epithelium of OLP patients: CD14, CXCL1, IL8, and TLR1, and at least two of these proteins, TLR1 and CXCL1, were expressed at substantial levels in oral keratinocytes. Because of the large accumulation of T cells in lesions of OLP it has long been thought to be an adaptive immunity malfunction. We provide evidence that there is increased expression of innate immune genes in the epithelium with this illness, suggesting a role for this process in the disease and a possible target for treatment.