脓疱型银屑病是免疫介导的炎症性皮肤病，Th17/Treg细胞免疫失衡是其发病可能的核心机制。近年来，免疫负向调节机制在维持炎症免疫稳态平衡中取得了较大进展。B10细胞属免疫负向调节细胞，在多种免疫介导的炎症性疾病中发挥重要作用。我们前期研究发现，脓疱型银屑病患者外周血B10细胞表达减少，IL-10低表达、IFN-γ和TNF-α则过度表达。银屑病小鼠模型皮下注射B10细胞后银屑病样皮损明显改善。本课题将在前期研究基础上，以B10细胞对Th17/Treg细胞免疫失衡的负向调节作用作为研究切入点，结合体内外实验探究B10细胞在脓疱型银屑病中的数量、表型、分化能力及功能，阐明B10细胞通过CD40-CD40L途径发挥免疫负向调节作用可能的机制，使用Card14E138A/+基因突变银屑病小鼠模型，挖掘B10细胞在皮损部位直接发挥抑制作用的可能性，为临床靶细胞治疗脓疱型银屑病提供理论与实验依据。

Pustular psoriasis is an immune-related inflammatory skin disease, and the imbalance of Th17/Treg cellular immunity is the core mechanism of its possible pathogenesis. In recent years, the negative immune regulation mechanism has made great progress in maintaining inflammatory immune homeostasis. B10 cells are one of the negative immune regulatory cells and play an important role in a variety of immune-related inflammatory diseases. Our previous research found that the expression of B10 cells in peripheral blood were reduced in patients with pustular psoriasis and low levels of IL-10, while IFN-γ and TNF-α were overexpressed. The psoriasis-like dermatitis were significantly improved after subcutaneous injection of B10 cells through the mouse model of psoriasis. Based on the former findings, our herein research focuses on negative regulation of B10 cells for the imbalance of Th17/Treg cellular immunity by means of in vitro and in vivo experiment, exploring the number, phenotype, ability of differentiation and function of B10 cells in pustular psoriasis, as well as clarifying the possible mechanism of negative immune regulation in B10 cells through the CD40-CD40L pathway. The Card14E138A / + genetically mutated psoriasis-like dermatitis mouse model will be used to explore the possibility of inhibitory effect of B10 cells in the lesion, which will provide the theoretical and experimental basis for clinical developments of B10-targeted pustular psoriasis-treating agents.