title: Adoptive transfer of bone marrow dendritic cells failed to localize in the renal cortex and to improve renal injury in adriamycin nephropathy.
abstract: OBJECTIVE
  Murine bone marrow (BM) dendritic cells (DCs) can be modulated to be tolerogenic by cytokines, such as interleukin (IL)-10 and transforming growth factor (TGF)-β, and may play a regulatory role and sustain immune hemostasis in cognate kidney disease. However, it is unknown whether BM-DCs can be used to protect against renal injury in murine Adriamycin nephropathy (AN).
  
  
  METHODS
  In this study, by adoptive in vivo transfer of BM-DCs, including immature DCs, mature DCs (lipopolysaccharide-stimulated DCs) and BM regulatory DCs (IL-10/TGF-β-modified DCs, DCregs), we addressed the potential benefits of BM-DCs in chronic kidney disease.
  
  
  RESULTS
  We found that after adoptive transfer of DCregs, renal injury, including glomerulosclerosis, interstitial fibrosis and tubular atrophy, was not changed compared to AN controls. Correspondingly, renal functions measured by serum creatinine, 12-hour urine protein and creatinine clearance were also not improved by transfusion with DCregs compared to AN controls.
  
  
  CONCLUSIONS
  This study showed that the adoptive transfer of BM-DCs was unable to improve renal injury in an AN model, and this failure related to their inability to access the kidney.
authors: Department of Nephrology, Shanghai 10th People's Hospital, Tongji University School of Medicine, Shanghai, China.
authors: Dong
authors: D
authors: Zheng
authors: Lei
authors: L
authors: Wen
authors: Changbin
authors: C
authors: Li
authors: Ai
authors: A
authors: Peng
authors: Qi
authors: Q
authors: Cao
authors: Yiping
authors: Y
authors: Wang
authors: David
authors: D
authors: Harris
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D018122:B7-1 Antigen / Q000276:immunology / Q000378:metabolism; D051940:B7-2 Antigen / Q000276:immunology / Q000378:metabolism; D001854:Bone Marrow Cells / Q000276:immunology / Q000378:metabolism; D002478:Cells, Cultured; D018925:Chemokines / Q000235:genetics / Q000276:immunology; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism / Q000637:transplantation; D004317:Doxorubicin; D005434:Flow Cytometry; D015870:Gene Expression / Q000276:immunology; D007672:Kidney Cortex / Q000276:immunology* / Q000378:metabolism; D007674:Kidney Diseases / Q000139:chemically induced / Q000276:immunology* / Q000628:therapy; D008070:Lipopolysaccharides / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D019707:Receptors, Chemokine / Q000235:genetics / Q000276:immunology; D051436:Renal Insufficiency, Chronic / Q000276:immunology* / Q000628:therapy; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017211:Treatment Failure
chemical_list: D018122:B7-1 Antigen; D051940:B7-2 Antigen; D018925:Chemokines; D016207:Cytokines; D008070:Lipopolysaccharides; D019707:Receptors, Chemokine; D004317:Doxorubicin