Dong Zheng, Lei Wen, Changbin Li, Ai Peng, Qi Cao, Yiping Wang, David Harris
{"title":"骨髓树突状细胞过继移植不能定位于肾皮质,也不能改善阿霉素肾病的肾损伤。","authors":"Dong Zheng, Lei Wen, Changbin Li, Ai Peng, Qi Cao, Yiping Wang, David Harris","doi":"10.1159/000358086","DOIUrl":null,"url":null,"abstract":"<p><strong>Background and aims: </strong>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).</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":18993,"journal":{"name":"Nephron Experimental Nephrology","volume":"126 1","pages":"8-15"},"PeriodicalIF":0.0000,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000358086","citationCount":"5","resultStr":"{\"title\":\"Adoptive transfer of bone marrow dendritic cells failed to localize in the renal cortex and to improve renal injury in adriamycin nephropathy.\",\"authors\":\"Dong Zheng, Lei Wen, Changbin Li, Ai Peng, Qi Cao, Yiping Wang, David Harris\",\"doi\":\"10.1159/000358086\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background and aims: </strong>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).</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>\",\"PeriodicalId\":18993,\"journal\":{\"name\":\"Nephron Experimental Nephrology\",\"volume\":\"126 1\",\"pages\":\"8-15\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2014-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1159/000358086\",\"citationCount\":\"5\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nephron Experimental Nephrology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1159/000358086\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2014/2/11 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nephron Experimental Nephrology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000358086","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2014/2/11 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
Adoptive transfer of bone marrow dendritic cells failed to localize in the renal cortex and to improve renal injury in adriamycin nephropathy.
Background and aims: 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.
Conclusion: 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.