为了研究4型肽基精氨酸脱亚胺酶(peptidyl arginine deimidase type 4, PAD4)在炎症脂肪组织中的作用及机制,分别提取db/db[Ⅱ型糖尿病(type 2 diabetes mellitus, T2DM)组]、db/m(T2DM对照组)、ob/ob(肥胖组)和ob/c(肥胖对照组)4组小鼠皮下和内脏脂肪组织，免疫组化技术检测PAD4在T2DM和肥胖小鼠皮下和内脏脂肪组织中的表达情况；LPS刺激野生型小鼠原代腹腔巨噬细胞和小鼠巨噬细胞系RAW264.7，qRT-PCR和Western blotting检测两种细胞中PAD4、炎性因子TNF-α和IL-6的表达以及NF-κB信号通路的激活情况。结果显示，与db/m、ob/c两组小鼠相比，db/db、ob/ob两组小鼠中皮下和内脏脂肪组织、经LPS刺激的小鼠原代腹腔巨噬细胞和RAW264.7细胞中PAD4的表达均降低，炎性因子TNF-α和IL-6的表达均明显升高；同时TLR4/NF-κB信号通路激活。该研究表明PAD4在炎症状态下(T2DM和肥胖)的皮下和内脏脂肪组织中表达下降，并与TLR4/NF-κB信号通路激活呈负相关。

Peripheral helper T cells (Tph) have been identified in recent years as a CD4⁺ T cell subset. Tph are characterized by the secretion of  C-X-C motif chemokine ligand 13 (CXCL13), and the expression of surface molecules including PD-1, inducible costimulatory  (ICOS), HLA-DR, etc. By expressing chemokine receptor C-C motif chemokine receptor 2 (CCR2), C-X3-C motif chemokine receptor 1 (CX3CR1), and CCR5, Tph can be recruited to inflammatory sites and promote the formation of tertiary lymphoid structures (TLS). Through interaction with IL-21 and signaling lymphocytic activation molecule family (SLAMF), Tph assist B cell maturation, differentiation, and antibody production. Tph are shown to be involved in the pathogenesis of many autoimmune diseases. Herein, this review discusses the biological characteristics of Tph and their role in different types of autoimmune diseases to further reveal their mechanism of action and clinical value, and provide new ideas for future targeted therapy.