Yiping Wang

ORCID: 0000-0003-0047-1825
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About
Contact & Profiles
Research Areas
  • Renal Diseases and Glomerulopathies
  • Immune cells in cancer
  • Chronic Kidney Disease and Diabetes
  • Reproductive System and Pregnancy
  • T-cell and B-cell Immunology
  • Dialysis and Renal Disease Management
  • Immune Cell Function and Interaction
  • Phagocytosis and Immune Regulation
  • Cancer-related molecular mechanisms research
  • Helicobacter pylori-related gastroenterology studies
  • Traditional Chinese Medicine Analysis
  • Esophageal and GI Pathology
  • Gastroesophageal reflux and treatments
  • MicroRNA in disease regulation
  • IL-33, ST2, and ILC Pathways
  • Gout, Hyperuricemia, Uric Acid
  • Acute Kidney Injury Research
  • Eosinophilic Esophagitis
  • Circular RNAs in diseases
  • Renal Transplantation Outcomes and Treatments
  • Inflammasome and immune disorders
  • Lipid metabolism and disorders
  • Immunotherapy and Immune Responses
  • Vasculitis and related conditions
  • Gastrointestinal Bleeding Diagnosis and Treatment

The University of Sydney
2014-2025

Shanghai Clinical Research Center
2025

Shanghai Jiao Tong University
2025

Shanghai First People's Hospital
2025

Westmead Institute for Medical Research
2014-2025

Sun Yat-sen University
2019-2025

Fifth Affiliated Hospital of Sun Yat-sen University
2019-2025

Anhui University of Traditional Chinese Medicine
2009-2024

Jilin Maternity and Child Health Care Hospital
2024

National Center on Addiction and Substance Abuse at Columbia University
2024

Two types of alternatively activated macrophages, M(2a) induced by IL-4/IL-13 and M(2c) IL-10/TGF-β, exhibit anti-inflammatory functions in vitro protect against renal injury vivo. Since their relative therapeutic efficacy is unclear, we compared the effects these two macrophage subsets murine adriamycin nephrosis. Both significantly reduced inflammation injury; however, macrophages more effectively glomerulosclerosis, tubular atrophy, interstitial expansion, proteinuria than macrophages....

10.1038/ki.2013.135 article EN publisher-specific-oa Kidney International 2013-05-01

IL-10/TGF-β–modified macrophages, a subset of activated produce anti-inflammatory cytokines, suggesting that they may protect against inflammation-mediated injury. Here, macrophages modified ex vivo by IL-10/TGF-β (IL-10/TGF-β Μ2) significantly attenuated renal inflammation, structural injury, and functional decline in murine adriamycin nephrosis (AN). These cells deactivated effector inhibited CD4+ T cell proliferation. Μ2 expressed high levels the regulatory co-stimulatory molecule B7-H4,...

10.1681/asn.2009060592 article EN Journal of the American Society of Nephrology 2010-03-19

Conventional markers of macrophages (Mфs) and dendritic cells (DCs) lack specificity often overlap, leading to confusion controversy regarding the precise function these in kidney other diseases. This study aimed identify phenotype renal mononuclear phagocytes (rMPs) expressing key both Mфs DCs. F4/80+CD11c+ accounted for 45% total rMPs normal kidneys those from mice with Adriamycin nephropathy (AN). Despite expression DC marker CD11c, double-positive displayed features Mфs, including...

10.1681/asn.2013121336 article EN Journal of the American Society of Nephrology 2014-07-11

<i>Background:</i> Alternatively activated macrophages (M2 macrophages) are able to reduce renal injury in murine adriamycin nephropathy. However, the effect of M2 other diseases such as diabetic nephropathy remains unknown. <i>Methods:</i> Macrophages were separated from splenocytes and polarized with IL-4 IL-13 into a protective phenotype. Mice underwent adoptive transfer macrophages, then diabetes was induced by tail vein injection streptozotocin (STZ). Blood...

10.1159/000321034 article EN Nephron Experimental Nephrology 2011-02-11

Chronic proteinuric renal injury is a major cause of ESRD. Adriamycin nephropathy murine model chronic disease whereby chemical followed by immune and structural changes that mimic human disease. Foxp3 gene induces regulatory T cell (Treg) phenotype. It was hypothesized Foxp3-transduced Treg could protect against in nephropathy. CD4+ cells were transduced with either Foxp3-containing retrovirus or control retrovirus. had phenotype functional phenotypic assays. Adoptive transfer protected...

10.1681/asn.2005090978 article EN Journal of the American Society of Nephrology 2006-02-09

The kidney contains receptors for the cytokine IL-25, but effects of IL-25 in CKD are unknown. Here, we induced adriamycin nephropathy both BALB/c mice and severe combined immunodeficient (SCID) mice, injected 7 consecutive days starting at day 5 after administration. treated with had less glomerulosclerosis, tubular atrophy, interstitial expansion, proteinuria than control 28. increased levels IL-4 IL-13 serum, kidney, renal draining lymph nodes, CD4+ lymphocytes. also directly suppressed...

10.1681/asn.2010070693 article EN Journal of the American Society of Nephrology 2011-07-01

Regulatory T cells (Tregs) help protect against autoimmune renal injury. The use of agonist antibodies and antibody/cytokine combinations to expand Tregs in vivo may have therapeutic potential for disease. Here, we investigated the effects administering IL-2/IL-2Ab complexes mice with adriamycin nephropathy, a model proteinuric kidney disease that resembles human focal segmental glomerulosclerosis. Injecting before or, lesser extent, after induction promoted expansion Tregs. Furthermore,...

10.1681/asn.2011111130 article EN Journal of the American Society of Nephrology 2012-06-08

CD103 + dendritic cells (DCs) in nonlymphoid organs exhibit two main functions: maintaining tolerance by induction of regulatory T and protecting against tissue infection through cross-presentation foreign antigens to CD8 cells. However, the role DCs kidney disease is unknown. In this study, we show that are one four subpopulations renal mononuclear phagocytes normal kidneys. expressed DC-specific surface markers, transcription factors, growth factor receptors were found cortex but not...

10.1681/asn.2015030229 article EN Journal of the American Society of Nephrology 2015-09-16
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