The pathogenetic role of kerationocytes in cutaneous lupus erythematosus

红斑狼疮(LE)是一种自身免疫性疾病，皮肤表现属于LE最常见的临床特征。到目前为止，还没有病因治疗方案。在一些患者中，慢性复发过程、建立不可逆转的疤痕皮肤缺损和脱发仍然不能令人满意地被免疫抑制治疗所控制。尽管进行了广泛的研究，但狼疮特异性皮损的发病机制尚不清楚。然而，开发有效的局部疗法的一个先决条件是更好地了解潜在的机制，并确定在未来的治疗中针对的关键因素。我们从不同的疾病中了解到，免疫调节介质的表达谱和作用可能存在显着差异，这取决于受影响的身体间隔。微环境的设置以及驻留细胞的特殊特征已被证明对免疫反应的结果非常重要。越来越多的证据表明，角质形成细胞在调节和维持皮肤红斑狼疮的病理过程中起着关键作用。这项研究的重点将放在角质形成细胞介体和角质形成细胞与存在于表皮基底层周围的淋巴细胞之间的相互作用上。病理生理机制，包括缺陷的清除凋亡细胞，热休克蛋白70，以及与效应和调节性T细胞的相互作用，将被详细研究。本研究的目的是明确表皮细胞在皮肤红斑狼疮的发生和维持中的作用。

Lupus erythematosus (LE) is an autoimmune disorder and the cutaneous manifestations belong to the most common clinical features of LE. To date there exists no causative treatment regimen. The chronic relapsing course, establishment of irreversible scarring skin defects and hair loss are still unsatisfactory controlled by immunosuppressive therapeutics in a number of patients. Despite extensive investigation, the pathogenesis of lupus-specific cutaneous lesions is unknown. However, a prerequisite for development of effective local therapeutics would be to better understand underlying mechanisms and to identify key factors to target in future therapies. We have learned from different diseases that marked differences of the expression profile and action of immunoregulatory mediators may exist depending on the body compartment affected. Micromilieu settings as well as particular features of resident cells have been shown to be of great importance for the outcome of the immune response. Evidence is accumulating that keratinocytes play a key role in regulating and maintaining the pathology in cutaneous LE. The focus of this study will be on keratinocyte mediators and keratinocyte dependent interactions with lymphocytes present in the surroundings of the epidermal basal layer. Pathophysiological mechanisms involving defective clearance of apoptotic cells, HSP70 and interaction with effector and regulatory T-cells will be examined in detail. It is the aim of this study to clearly define the contribution of resident epidermal cells to the onset and maintenance of cutaneous LE.