Büchau Amanda S, Gallo Richard L
Department of Medicine, Division of Dermatology, University of California at San Diego School of Medicine, San Diego, CA 92161, USA.
Clin Dermatol. 2007 Nov-Dec;25(6):616-24. doi: 10.1016/j.clindermatol.2007.08.016.
Psoriasis is a chronic inflammatory disorder that is mediated by elements of the innate and adaptive immune systems. Its characteristic features in the skin consist of inflammatory changes in both dermis and epidermis, with abnormal keratinocyte differentiation and proliferation. Despite the elucidation of many aspects of psoriasis pathogenesis, some puzzling questions remain to be answered. A major question currently debated is whether psoriasis is a primary abnormality of the epidermal keratinocyte or a reflection of dysregulated bone marrow-derived immunocytes. In this review we will focus on understanding the role of the innate immune system in psoriasis and how this provides a rational solution to address the origin of this multifactorial disease. Innate immunity is nonspecific and genetically based. It protects the body against the constant risk of pathogens through the use of rapidly mobilized defenses that are able to recognize and kill a variety of threats (bacteria, fungi, viruses, etc). The key mechanisms of innate immune responses are the existence of receptors to recognize pathogens and the production of factors that kill pathogens, such as antimicrobial peptides and proteins. Any combination of excessive sensitivity of the innate detection system, or dysregulation of the response system, can manifest both an epidermal phenotype and an abnormal T-cell function. Thus, the multidimensional action of the innate immune system, its triggers, and its recently understood role in T-cell function argue for an important role for innate mechanisms of recognition and response in the pathogenesis of psoriasis.
银屑病是一种慢性炎症性疾病，由先天性和适应性免疫系统的成分介导。其皮肤的特征性表现包括真皮和表皮的炎症变化，伴有角质形成细胞异常分化和增殖。尽管对银屑病发病机制的许多方面已有阐明，但仍有一些令人困惑的问题有待解答。目前正在争论的一个主要问题是，银屑病是表皮角质形成细胞的原发性异常，还是骨髓来源的免疫细胞失调的反映。在这篇综述中，我们将着重理解先天性免疫系统在银屑病中的作用，以及这如何为解决这种多因素疾病的起源提供合理的解释。先天性免疫是非特异性的且基于遗传。它通过利用能够识别和杀死各种威胁（细菌、真菌、病毒等）的快速动员的防御机制，保护身体免受病原体的持续威胁。先天性免疫反应 的关键机制是存在识别病原体的受体以及产生杀死病原体的因子，如抗菌肽和蛋白质。先天性检测系统的过度敏感或反应系统的失调的任何组合，都可能表现出表皮表型和异常的T细胞功能。因此，先天性免疫系统的多维度作用、其触发因素以及其最近被理解的在T细胞功能中的作用，都表明先天性识别和反应机制在银屑病发病机制中起重要作用。
