The Plastic Surgery Foundation
Log In Donate Now

Grants We Funded

Grant applicants for the 2022 cycle requested a total of over $2.9 million dollars. The PSF Study Section subcommittees of Basic & Translational Research and Clinical Research evaluated 115 grant applications on the following topics:

The PSF awarded research grants totaling almost $550,000 to support 19 plastic surgery research proposals.

ASPS/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.

Role of Schwann Cell CD-40 Status on Nerve Allograft Rejection

Principal Investigator
Debbie Yu MD


University of Michigan

Funding Mechanism
Basic Research Grant

Focus Area
Peripheral Nerve

Peripheral nerve injuries are frequently seen by plastic surgeons. While it is known that the best result is obtained when those nerve gaps are repaired with auto grafts, auto grafts sometimes may not provide adequate amounts of nerve for reconstruction of long or complex defects (Rodriguez et al. 2000). Tissue-engineered grafts, such as acellularized peripheral nerve grafts, provide a possible solution for reconstruction of gaps less than 2 cm in length (Haase et al. 2003). Unfortunately, no tissue-engineered constructs are efficacious for long (>6 cm) nerve gaps. Peripheral nerve allografts are a potential alternative for reconstruction of long gaps but are limited in their clinical utility due to the need for nonspecific, global immunosuppression. Specifically, the allograft Schwann cells (SCs) behave as antigen-presenting cells leading to cell death and rejection without immunosuppression (Trumble and Shon 2000). Significant attention has been directed towards targeting co-stimulatory pathways as inductive therapy for reducing alloimmune responses and preventing allograft rejection. The CD40-CD40L pathway has received the most academic scrutiny and seems to play a prominent role in T-cell-mediated rejection (Harlan 1999). Blockade of this pathway has been found to produce a permissive state in murine peripheral nerve allografts (Brenner et al. 2004). Strategies to induce tolerance or long-term immunologic hyporesponsiveness following nerve allografting require a better understanding of which SCs populate a nerve allograft in the setting of costimulatory pathway blockade with MRl after nerve-gap reconstruction: donor or recipient SCs. Our hypothesis is that donor nerve SCs do not survive allotransplantation and are rejected if they are not given immunosuppression and that the transplanted nerve graft is repopulated with autogenous or recipient SCs. Under conditions of CD40lCD40L co-stimulatory pathway blockade, there will likely exist a combination of autogenous and donor SCs within the transplanted nerve. If this hypothesis is correct, successful nerve regeneration in long nerve grafts will then require that tolerance or a permissive state must be established in the recipient through co-stimulatory pathway blockade to prevent rejection of the remaining SCs. If the entire allograft ultimately is replaced with autogenous SCs, then only temporary immunosuppression is required until all allograft SCs have been eliminated. Once the source of the SCs is clear, variables can then be manipulated to effect nerve regeneration.