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Insights from immunoproteomic profiling of a rejected full-face transplant
CAA. Lee, D. Wang, M. Kauke-Navarro, E. Russell-Goldman, S. Xu, KN. Mucciarone, S. Sohrabi, CG. Lian, B. Pomahac, GF. Murphy
Language English Country United States
Document type Case Reports, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't
Grant support
R01 HL161087
NHLBI NIH HHS - United States
- MeSH
- Graft Survival MeSH
- Proteomics MeSH
- Graft Rejection etiology pathology MeSH
- Composite Tissue Allografts * transplantation MeSH
- Facial Transplantation * MeSH
- Vascularized Composite Allotransplantation * MeSH
- Publication type
- Case Reports MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, N.I.H., Extramural MeSH
Vascularized composite allografts (VCAs) of faces and extremities are subject to chronic rejection that is incompletely understood. Here we report on immunoproteomic evaluation of a full facial VCA removed 88 months after transplantation due to chronic rejection. CD8-positive T cells of donor (graft) origin infiltrate deep intragraft arteries in apposition to degenerating endothelium of chimeric recipient origin in association with arteriosclerotic alterations. Digital spatial proteomic profiling highlighted proteins expressed by activated cytotoxic T cells and macrophages as well as pathway components involved in atherogenic responses, including Indoleamine 2,3-Dioxygenase 1 (IDO1) and Stimulator of Interferon Response CGAMP Interactor (STING). Chronic facial VCA rejection thus involves T cell/macrophage-mediated accelerated arteriosclerosis not normally represented in punch biopsies and potentially driven by persistent graft-resident effector T cells and recipient target endothelium that chimerically repopulates graft arteries.
Department of Pathology Brigham and Women's Hospital Boston Massachusetts USA
Department of Surgery Yale School of Medicine New Haven Connecticut USA
References provided by Crossref.org
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- $a Vascularized composite allografts (VCAs) of faces and extremities are subject to chronic rejection that is incompletely understood. Here we report on immunoproteomic evaluation of a full facial VCA removed 88 months after transplantation due to chronic rejection. CD8-positive T cells of donor (graft) origin infiltrate deep intragraft arteries in apposition to degenerating endothelium of chimeric recipient origin in association with arteriosclerotic alterations. Digital spatial proteomic profiling highlighted proteins expressed by activated cytotoxic T cells and macrophages as well as pathway components involved in atherogenic responses, including Indoleamine 2,3-Dioxygenase 1 (IDO1) and Stimulator of Interferon Response CGAMP Interactor (STING). Chronic facial VCA rejection thus involves T cell/macrophage-mediated accelerated arteriosclerosis not normally represented in punch biopsies and potentially driven by persistent graft-resident effector T cells and recipient target endothelium that chimerically repopulates graft arteries.
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