Th17/Treg平衡失调在IgA肾病中的作用机制与临床转化OA

IgA nephropathy(IgAN)is one of the most prevalent primary glomerular diseases worldwide and represents the leading primary cause of end-stage renal disease(ESRD)in China.Approximately 20％to 40％of patients with IgAN progress to ESRD within 10 to 20 years after diagnosis.Recent studies have revealed that immune dysregulation is a central mechanism underlying the pathogenesis of IgAN.Among the various immune abnormalities,an imbalance between helper T cell 17 cells(Th17)and regulatory T cells(Treg)has emerged as a critical driver of inflammatory progression and renal injury.Th17 cells promote the production of galactose-deficient IgA1(Gd-IgA1)through the secretion of pro-inflammatory cytokines such as interleukin(IL)-17,thereby activating local renal inflammation and fibrosis.In contrast,Treg cells exert renoprotective effects by suppressing excessive immune activation through the secretion of anti-inflammatory cytokines,including IL-10 and transforming growth factor-β(TGF-β).A comprehensive review of the regulatory networks,underlying mechanisms,and clinical translational significance of Th17/Treg imbalance in IgAN may contribute to a deeper understanding of the molecular mechanisms governing Th17/Treg homeostasis,facilitate the development of precise-targeted therapies and individualized intervention strategies,and ultimately improve the long-term prognosis of patients with IgAN.