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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
Jazyk angličtina Země Spojené státy americké
Typ dokumentu kazuistiky, Research Support, N.I.H., Extramural, práce podpořená grantem
Grantová podpora
R01 HL161087
NHLBI NIH HHS - United States
- MeSH
- přežívání štěpu MeSH
- proteomika MeSH
- rejekce štěpu etiologie patologie MeSH
- štěpy z kompozitní tkáně * transplantace MeSH
- transplantace obličeje * MeSH
- vaskularizovaná kompozitní alotransplantace * MeSH
- Publikační typ
- kazuistiky MeSH
- práce podpořená grantem 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
Citace poskytuje 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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