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In JoVE (3)
- A Novel Microsurgical Model for Heterotopic, En Bloc Chest Wall, Thymus, and Heart Transplantation in Mice
- Orthotopic Hind Limb Transplantation in the Mouse
- Murine Full-thickness Skin Transplantation
Other Publications (3)
Articles by Byoungchol Oh in JoVE
A Novel Microsurgical Model for Heterotopic, En Bloc Chest Wall, Thymus, and Heart Transplantation in Mice
Byoungchol Oh*1, Georg J. Furtmüller*1, Michael Sosin*1, Madeline L. Fryer1, Lawrence J. Gottlieb2,3, Michael R. Christy4, Gerald Brandacher1,5,6, Amir H. Dorafshar1,5,6
1Johns Hopkins University School of Medicine, 2Burn and Complex Wound Center, 3Section of Plastic and Reconstructive Surgery, University of Chicago Medical Center, 4Division of Plastic, Reconstructive, and Maxillofacial Surgery, R Adams Cowley Shock Trauma Center, 5Department of Plastic and Reconstructive Surgery, Johns Hopkins University School of Medicine, 6Vascularized Composite Allotransplantation (VCA) Lab, Johns Hopkins University School of Medicine
Orthotopic Hind Limb Transplantation in the Mouse
Georg J. Furtmüller*1, Byoungchol Oh*1, Johanna Grahammer*2, Cheng-Hung Lin3, Robert Sucher4, Madeline L. Fryer1, Giorgio Raimondi1, W.P. Andrew Lee1, Gerald Brandacher1
1Department of Plastic and Reconstructive Surgery, Vascularized Composite Allotransplantation (VCA) Laboratory, Johns Hopkins University School of Medicine, 2Department of Visceral, Transplant and Thoracic Surgery, Innsbruck Medical University, 3Center for Vascularized Composite Allotransplantation, Department of Plastic and Reconstructive Surgery, Chang Gung Memorial Hospital and School of Medicine, 4Department of General, Visceral and Transplant Surgery, Charite Berlin
Murine Full-thickness Skin Transplantation
Chih-Hsien Cheng*1,2, Chen-Fang Lee*1,2, Madeline Fryer*3, Georg J. Furtmüller3, Byoungchol Oh3, Jonathan D. Powell1, Gerald Brandacher3
1Sidney-Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, 2Department of Liver and Transplantation Surgery, Chang-Gung Transplantation Institute, Chang-Gung Memorial Hospital, Chang-Gung University College of Medicine, 3Vascularized Composite Allotransplantation Laboratory, Department of Plastic and Reconstructive Surgery, Johns Hopkins University School of Medicine
Other articles by Byoungchol Oh on PubMed
Seminars in Immunology. Apr, 2012 | Pubmed ID: 22137187
The role of antibodies in chronic injury to organ transplants has been suggested for many years, but recently emphasized by new data. We have observed that when immunosuppressive potency decreases either by intentional weaning of maintenance agents or due to homeostatic repopulation after immune cell depletion, the threshold of B cell activation may be lowered. In human transplant recipients the result may be donor-specific antibody, C4d+ injury, and chronic rejection. This scenario has precise parallels in a rhesus monkey renal allograft model in which T cells are depleted with CD3 immunotoxin, or in a CD52-T cell transgenic mouse model using alemtuzumab to deplete T cells. Such animal models may be useful for the testing of therapeutic strategies to prevent DSA. We agree with others who suggest that weaning of immunosuppression may place transplant recipients at risk of chronic antibody-mediated rejection, and that strategies to prevent this scenario are needed if we are to improve long-term graft and patient outcomes in transplantation. We believe that animal models will play a crucial role in defining the pathophysiology of antibody-mediated rejection and in developing effective therapies to prevent graft injury. Two such animal models are described herein.
Cold Spring Harbor Perspectives in Medicine. Jul, 2013 | Pubmed ID: 23818516
Because lymphocytes were shown to mediate transplant rejection, their depletion has been studied as a mechanism of preventing rejection and perhaps inducing immunologic tolerance. Agents that profoundly deplete lymphocytes have included monoclonal antibodies, cytotoxic drugs, and radiation. We have studied several such agents but focused on antibodies that deplete not only peripheral blood lymphocytes, but also lymph node lymphocytes. Depletion of lymph node T lymphocytes appears to permit peripheral tolerance at least for T cells in animal models. Nevertheless, B-cell responses may be resistant to such approaches, and T memory cells are likewise relatively resistant to depleting antibodies. We review the experimental and clinical approaches to depletion strategies and outline some of the pitfalls of depletion, such as limitations of currently available agents, duration of tolerance, infection, and malignancy. It is notable that most tolerogenic strategies that have been attempted experimentally and clinically include depleting agents even when they are not named as the underlying strategy. Thus, there is an implicitly acknowledged role for reducing the precursor frequency of donor antigen-specific lymphocytes when approaching the daunting goal of transplant tolerance.
Cell Reports. Oct, 2015 | Pubmed ID: 26489460
Upon antigen recognition and co-stimulation, T lymphocytes upregulate the metabolic machinery necessary to proliferate and sustain effector function. This metabolic reprogramming in T cells regulates T cell activation and differentiation but is not just a consequence of antigen recognition. Although such metabolic reprogramming promotes the differentiation and function of T effector cells, the differentiation of regulatory T cells employs different metabolic reprogramming. Therefore, we hypothesized that inhibition of glycolysis and glutamine metabolism might prevent graft rejection by inhibiting effector generation and function and promoting regulatory T cell generation. We devised an anti-rejection regimen involving the glycolytic inhibitor 2-deoxyglucose (2-DG), the anti-type II diabetes drug metformin, and the inhibitor of glutamine metabolism 6-diazo-5-oxo-L-norleucine (DON). Using this triple-drug regimen, we were able to prevent or delay graft rejection in fully mismatched skin and heart allograft transplantation models.