Depletion of Fractalkine ameliorates renal injury and Treg cell apoptosis via the p38MAPK pathway in lupus-prone mice

Fractalkine (FKN) is a chemokine with several roles, including chemotaxis; adhesion; and immune damage, which also participates in cell inflammation apoptosis responds to the pathogenesis of autoimmune diseases. Given involvement regulatory T cells (Treg) diseases, this study investigated mechanism FKN renal injury Treg via p38 mitogen-activated protein kinase (p38MAPK) signaling pathway lupus-prone mice. Lupus was induced BALB/c female mice by injection pristane, followed isolation CD4+CD25+ from spleen lupus model To deplete FKN, received an anti-FKN antibody, were transfected small-interfering RNA. treated p38MAPK inhibitor SB203580 activator U-46619, respectively, urine serum urea nitrogen, creatinine, autoantibodies measured histopathological changes analyzed. We determined levels phosphorylated (p-p38), forkhead box P3 (FOXP3) tissue cells, analyzed rates key apoptotic factors cells. The p-p38 increased, whereas FOXP3 level decreased Treatment antibody ameliorated proteinuria function, significantly reducing autoantibody, while increasing Moreover, knockdown administration reduced pro-apoptotic factors, increased anti-apoptotic suppressed activation derived Furthermore, treatment U-46619 had opposite effect on these These data indicated that depletion inhibition nephritis, suggesting targeting represents potential therapeutic strategy for treating nephritis.