1. Age and Immune Response:
We have identified immunosenescence as a criticial component affecting both rejection and tolerance:
Specific Projects:
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Memory T cell function in aged mice: while numbers of T cells with a memory phenotype increase with age, their functional capacity is compromised. We dissect memorallospecific memory T cell immune response on a molecular level.
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T cell exhaustion is playing a key role in immune responses. Age may accelerate 'physiological' T cell exhaustion with relevance to rejection an tolerance.
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Tolerance protocol in aged transplant recipients: our previous work shows an imparied alloimmune response in the aged animals. This project is to explore and establish immunosuppression protocols suitable for aged transplant recipients.
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We have observed that tolerance protocols work in an age-dependent way and are currently investigating the influence of recipient age on the outcome of allogeneic bone marrow transplantation for the purpose of mixed chimerism and tolerance induction.
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Donor-age accelerates the recipient's immune response. We have identified Dendritic cells as key players communicating the more potent immune response to older donor organs. We are currently dissecting age-specific migration and antigen presentation capacitites of DCs.
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Inflammatory consequences of Brain death: we have an established brain dead model in the mouse and are currntly dissecting the consequences of inflammatory activation following brain death in genetically modified mouse strains.
2. MicroRNA expression and ischemia-reperfusion injury:
3. Pulsatile flow and endothelial injury:
With clinical results demonstrating an improved organ preservation with pulsatile perfusion we study the role of endothelial injury on organ injury and rejection:
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This page was last modified on 1/30/2012