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This study investigates the therapeutic potential and mechanisms of paeoniflorin\u20106\n                      <jats:bold>\u2032<\/jats:bold>\n                      \u2010O\u2010benzene sulfonate (CP\u201025) to DCs in DKD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>DKD mouse model was established by high\u2010fat (HFD) feeding combined with intraperitoneal streptozotocin (STZ) injection. Renal histopathological changes were assessed via haematoxylin and eosin (H&amp;E), masson, and periodic acid\u2010schiff (PAS) staining. Renal function, oxidative stress, and lipid were also quantified. Immune cell differentiation and function were analysed by flow cytometry (FCM). The expression of renal injury markers and fibrosis\u2010associated mRNA and proteins were evaluated by quantitative real\u2010time PCR (qPCR) and western blotting. The target G protein\u2010coupled receptor kinase 2 (GRK2), PI3K\u2010AKT\u2013mTOR, and JAK2\u2010STAT3\u2010SOCS3 pathways were examined to analyse the mechanism of CP\u201025 to DKD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      CP\u201025 alleviated renal histopathological damage, inflammatory infiltration, and fibrosis in DKD. CP\u201025 also reversed renal function, lipid, and oxidative stress indicators of DKD. Additionally, CP\u201025 inhibited pro\u2010inflammatory cytokines (IL\u201012) and promoted anti\u2010inflammatory cytokines (IL\u20104 and IL\u201010) secretion in the serum of DKD. CP\u201025 inhibited the differentiation of CD103\n                      <jats:sup>+<\/jats:sup>\n                      DCs and the maturity of DCs in the bone marrow and kidney. Subsequently, CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cells in the spleen and kidney, NKT in the spleen, and T\n                      <jats:sub>regs<\/jats:sub>\n                      in the spleen and kidney of DKD mice were inhibited by CP\u201025 treatment. Other immune cells in other immune organs were less affected by CP\u201025. The communication of DC and T cell was down\u2010regulated by CP\u201025. The specific mechanism involved CP\u201025 targeting GRK2 to inhibit the JAK2\u2010STAT3\u2010SOCS3 pathway, thereby suppressing DC maturation and T cell communication in the renal inflammatory response to treat DKD. However, the inhibition of CP\u201025 to PI3K was indistinctive.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>CP\u201025 exhibits therapeutic efficacy against kidney injury in DKD. Its primary mechanism involves modulating the differentiation and function of DCs, which affects the activation of T cells. In terms of mechanism, CP\u201025 targets the GRK2\u2010mediated JAK2\u2010STAT3\u2010SOCS3 signalling pathway to inhibit inflammation for alleviating DKD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/1440-1681.70124","type":"journal-article","created":{"date-parts":[[2026,4,13]],"date-time":"2026-04-13T04:16:29Z","timestamp":1776053789000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Paeoniflorin\u20106\u2032\u2010O\u2010Benzenesulfonate Mediates Dendritic Cell Differentiation to Alleviate Diabetic Kidney Disease"],"prefix":"10.1111","volume":"53","author":[{"given":"Wei","family":"Liang","sequence":"first","affiliation":[{"name":"Department of Pharmacy The First Affiliated Hospital of Anhui Medical University, the Grade 3 Pharmaceutical Chemistry Laboratory of State Administration of Traditional Chinese Medicine  Hefei China"},{"name":"Department of Pharmacy Shanghai Hudong Hospital  Shanghai 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