Abstract: Nephrotic syndrome (NS) is a clinical syndrome characterized by massive proteinuria. With its global incidence steadily rising, current therapeutic strategies primarily rely on glucocorticoids and immunosuppressants. However, a subset of patients is prone to developing steroid resistance or experiencing disease relapse. Podocyte injury represents the core mechanism underlying proteinuria in NS. In recent years, significant attention has focused on the functions of immune checkpoint molecules B7⁃1 and PD⁃L1 in podocytes, with growing interest in their cis⁃interaction on the podocytes surface. This review systematically elaborates on the molecular basis, mechanisms of action, cis⁃interaction mechanisms, and recent advances in targeted therapies related to B7⁃1 and PD⁃L1. It provides novel insights into precision immunotherapy for NS, thereby facilitating the translation of mechanistic research into clinical applications.

Key words: nephrotic syndrome, B7 homolog 1, programmed death?ligand 1, cis?interaction