系统性红斑狼疮(SLE)是一种系统性自身免疫性疾病,由对内源性核抗原(如双链DNA)的耐受性丧失引起,导致T细胞的增殖和随后的B细胞的活化,导致严重的器官损伤和危及生命的并发症,如狼疮性肾炎。狼疮肾炎(LN)发展为SLE的常见并发症,占SLE病例的60%以上,以蛋白尿和异质性组织病理学结果为特征。肾小球损伤在蛋白尿中起作用,因为足细胞损伤是主要原因。许多研究已经报道,足细胞参与促进LN进展的免疫应答。在LN,免疫复合物沉积刺激树突状细胞分泌激活T细胞和B细胞的炎性细胞因子。B细胞分泌攻击和损害肾足细胞的自身抗体,导致肾足细胞损伤。受损的足细胞通过表达Toll样受体触发炎症细胞,并通过主要组织相容性复合物和CD86触发T细胞,从而参与局部免疫反应和足细胞损伤的加剧。在现有文献的基础上,本文综述了LN中足细胞在肾脏局部免疫微环境下的研究进展,探讨免疫微环境下足细胞损伤的机制,并评估足细胞作为LN的潜在治疗靶标。
Systemic lupus erythematosus (SLE) is a systemic autoimmune disorder caused by the loss of tolerance to endogenous nuclear antigens such as double‑stranded DNA, leading to the proliferation of T cells and subsequent activation of B cells, which results in serious organ damage and life‑threatening complications such as lupus nephritis. Lupus nephritis (LN) develops as a frequent complication of SLE, accounting for >60% of SLE cases, and is characterized by proteinuria and heterogeneous histopathological findings. Glomerular injury serves a role in proteinuria as podocyte damage is the leading contributor. Numerous studies have reported that
podocytes are involved in the immune response that promotes LN progression. In LN, immune complex deposition stimulates dendritic cells to secrete inflammatory cytokines that activate T cells and B cells. B cells secrete autoantibodies that attack and damage the renal
podocytes, leading to renal podocyte injury. The injured
podocytes trigger inflammatory cells through the expression of toll‑like receptors and trigger T cells through major histocompatibility complexes and CD86, thereby participating in the local immune response and the exacerbation of podocyte injury. Based on the existing literature, the present
review summarizes the research progress of
podocytes in LN under the local immune microenvironment of the kidney, explores the mechanism of podocyte injury under the immune microenvironment, and evaluates
podocytes as a potential therapeutic target for LN.