The Plastic Surgery Foundation
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Grants We Funded

In 2019, The Plastic Surgery Foundation (The PSF) awarded 33 investigator-initiated projects and allocated $891,274 to support the newest, clinically relevant research in plastic surgery.

The American Society of Plastic Surgeons/PSF leadership is committed to continuing to provide high levels of investigator-initiated research support to ensure that plastic surgeons have the needed research resources to be pioneers and innovators in advancing the practice of medicine.

Research Abstracts

Search The PSF database to have easy access to full-text grant abstracts from past PSF-funded research projects 2003 to present. All abstracts are the work of the Principal Investigators and were retrieved from their PSF grant applications. Several different filters may be applied to locate abstracts specific to a particular focus area, or PSF funding mechanism.

Induction of Nerve Allograft Tolerance Using anti-CD40L Monoclonal Antibody

Principal Investigator
Paul Cederna MD

Year
2003

Institution
University of Michigan

Funding Mechanism
Basic Research Grant

Focus Area
Peripheral Nerve

Abstract
Options for reconstruction of peripheral nerve gaps are currently limited. In clinical practice, long nerve gaps following injury or tumor resection that cannot be repaired primarily are repaired with autologous nerve grafts. This procedure requires sacrifice of healthy nerve with permanent functional impairment. In some clinical situations, there may not be sufficient autologous nerve available for reconstruction of larger, more complex nerve defects. As a result some investigators and clinicians have turned to peripheral nerve allografting as an alternative. The main obstacle to widespread clinical use of peripheral nerve allografts however has been T cell mediated immune rejection. Although potent immunosuppressive drugs are currently available to prevent graft rejection, they are associated with many toxicities. In addition, chronic global suppression of the immune system with these medications may result in opportunistic infections or secondary malignancies. Therefore more selective immunomodulatory strategies to prevent graft rejection of peripheral nerve allografts such as induction of specific immune tolerance will need to be developed before this technique can be routinely used clinically. The CD40-CD40L costimulatory pathway has been shown to play a crucial role in allograft rejection. CD40 is a 50-kDa membrane glycoprotein found on a variety of antigen-presenting cells of grafted tissue. The ligand for this membrane receptor is CD40L, a 39-kDa glycoprotein that is preferentially expressed on activated CD4+ T helper cells of the recipient. The CD40-CD40L interaction mediates T cell immune responses by enhancing the costimulatory pathway which leads to rejection. Manipulation of the CD40-CD40L co-stimulatory pathway may be beneficial in preventing allograft rejection. Indeed, consistent with its central role in cell mediated immunity, blockade of CD40- CD40L by anti-CD40L monoclonal antibody (mAb) has been shown to prevent rejection of solid organ transplants such as cardiac and renal allografts. However, the effect of blocking the CD40-CD40L pathway on the fate of peripheral nerve allografts has not been determined. The purpose of this project is to determine the effectiveness of anti-CD40L mAb treatment as a method to induce tolerance to peripheral nerve allografts.