银屑病是一种最常见的慢性炎症性皮肤病,复发缓解过程。最近几十年的深入研究揭示了银屑病发病机制中免疫细胞与其他类型细胞之间相互作用的病理网络。新的证据表明树突状细胞,TH17细胞,角质形成细胞构成牛皮癣的致病三联体。树突状细胞产生TNF-α和IL-23,以促进T细胞向TH17细胞分化,产生关键的银屑病细胞因子IL-17,IFN-γ,IL-22它们的活性导致皮肤炎症和角质形成细胞的活化和过度增殖。此外,其他细胞和信号通路与银屑病的发病机制有关,包括TH9细胞,TH22细胞,CD8+细胞毒性细胞,中性粒细胞,γδT细胞,以及它们分泌的细胞因子和趋化因子。来自病灶皮肤高通量分析的新见解鉴定了参与发病机制的新信号通路和细胞群。这些研究不仅扩大了我们对免疫反应机制和银屑病发病机理的认识,而且导致了银屑病患者临床管理的革命。因此,了解银屑病炎症的免疫反应机制对进一步研究至关重要,开发新的治疗策略,和银屑病患者的临床管理。该综述的目的是全面介绍牛皮癣中免疫反应的失调,重点是最近的发现。这里,我们描述了免疫细胞的作用,包括T细胞,B细胞,树突状细胞,中性粒细胞,单核细胞,肥大细胞,和先天淋巴样细胞(ILC),以及非免疫细胞,包括角质形成细胞,成纤维细胞,内皮细胞,和开始时的血小板,发展,和牛皮癣的进展。
Psoriasis is one of the most common inflammatory skin diseases with a chronic, relapsing-remitting course. The last decades of intense research uncovered a pathological network of interactions between immune cells and other types of cells in the pathogenesis of psoriasis. Emerging evidence indicates that dendritic cells, TH17 cells, and keratinocytes constitute a pathogenic triad in psoriasis. Dendritic cells produce TNF-α and IL-23 to promote T cell differentiation toward TH17 cells that produce key psoriatic cytokines IL-17, IFN-γ, and IL-22. Their activity results in skin inflammation and activation and hyperproliferation of keratinocytes. In addition, other cells and signaling pathways are implicated in the pathogenesis of psoriasis, including TH9 cells, TH22 cells, CD8+ cytotoxic cells, neutrophils, γδ T cells, and cytokines and chemokines secreted by them. New insights from high-throughput analysis of lesional skin identified novel signaling pathways and cell populations involved in the pathogenesis. These studies not only expanded our knowledge about the mechanisms of immune response and the pathogenesis of psoriasis but also resulted in a revolution in the clinical management of patients with psoriasis. Thus, understanding the mechanisms of immune response in psoriatic inflammation is crucial for further studies, the development of novel therapeutic strategies, and the clinical management of psoriasis patients. The aim of the review was to comprehensively present the dysregulation of immune response in psoriasis with an emphasis on recent findings. Here, we described the role of immune cells, including T cells, B cells, dendritic cells, neutrophils, monocytes, mast cells, and innate lymphoid cells (ILCs), as well as non-immune cells, including keratinocytes, fibroblasts, endothelial cells, and platelets in the initiation, development, and progression of psoriasis.