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首页> 外文期刊>Pathobiology: journal of immunopathology, molecular and cellular biology >Expression of lymphotoxin-alpha by keratinocytes: a further mediator for the lichenoid reaction.
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Expression of lymphotoxin-alpha by keratinocytes: a further mediator for the lichenoid reaction.

机译：角质形成细胞表达淋巴毒素：地衣样反应的另一种介质。

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OBJECTIVE: Lichen planus (LP) represents a disease in which autoimmune mechanisms mediated by Th1 T cells are involved. Lymphotoxin-alpha (LT-alpha) represents a Th1 cytokine with proinflammatory activities in LP, as has recently been demonstrated for interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha). METHODS: Expression of LT-alpha mRNA was investigated by RT-PCR and nonradioactive in situ hybridization. Double staining methods were applied to characterize the phenotype of cells expressing LT-alpha. Cell stimulation experiments were performed on the transformed squamous cell line HaCaT. RESULTS: In contrast to normal skin, LT-alpha-specific RT-PCR products were found in all cases of LP. Cells in the inflammatory infiltrate expressing LT-alpha were identified as mainly T cells and mast cells, as shown by in situ hybridization. Furthermore, predominant LT-alpha mRNA expression could be observed in lesional keratinocytes adjacent to the band-like inflammatory infiltrate. In cell stimulation experiments, it could be shown that IFN-gamma induces LT-alpha and TNF-alpha mRNA in the human squamous cell line HaCaT, concomitant with upregulation of MHC class II and intercellular adhesion molecule-1, which could also be observed on lesional keratinocytes in LP. CONCLUSIONS: In LP, LT-alpha mRNA is predominantly expressed by lesional keratinocytes and to a lesser extent by inflammatory cells. Induction of LT-alpha in keratinocytes is closely related to the expression of TNF-alpha and MHC class II. The loci of TNF-alpha and LT-alpha map to MHC class III on chromosome 6, which is closely linked to the MHC class II gene locus. Our results suggest that stimulation of keratinocytes with IFN-gamma results in the upregulation of proinflammatory cytokines such as LT-alpha and TNF-alpha as well as MHC class II, which map to the same gene region of immunoregulatory genes on chromosome 6 and may be involved in the induction and maintenance of the disease. Copyright 2001 S. Karger AG, Basel
机译：目的：扁平苔藓（LP）代表一种涉及Th1 T细胞介导的自身免疫机制的疾病。 Lymphotoxin-alpha（LT-alpha）代表在LP中具有促炎活性的Th1细胞因子，最近已经证明了干扰素-γ（IFN-γ）和肿瘤坏死因子-α（TNF-alpha）。方法：采用RT-PCR和非放射性原位杂交技术检测LT-αmRNA的表达。应用双重染色方法表征表达LT-α的细胞的表型。在转化的鳞状细胞系HaCaT上进行细胞刺激实验。结果：与正常皮肤相反，在所有LP病例中均发现了LT-α特异性RT-PCR产物。如原位杂交所示，表达炎性浸润的LT-α中的细胞主要被鉴定为T细胞和肥大细胞。此外，在与带状炎性浸润物相邻的病变角质形成细胞中可以观察到主要的LT-αmRNA表达。在细胞刺激实验中，可以证明IFN-γ诱导人鳞状细胞系HaCaT中的LT-α和TNF-αmRNA，并伴随着MHC II类和细胞间粘附分子-1的上调，这在LP中的病变角质形成细胞。结论：在LP中，LT-αmRNA主要由病变角质形成细胞表达，而在较小程度上由炎性细胞表达。角质形成细胞中LT-α的诱导与TNF-α和II类MHC的表达密切相关。 TNF-α和LT-α的基因座对应于6号染色体上的MHC III类，它与MHC II类基因位点紧密相连。我们的结果表明，用IFN-γ刺激角质形成细胞会导致促炎性细胞因子（如LT-α和TNF-α以及MHC II类）的上调，它们映射到6号染色体上免疫调节基因的相同基因区域，并且可能是参与疾病的诱导和维持。版权所有2001 S. Karger AG，巴塞尔

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