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Role of endothelial cells in graft-versus-host disease

To date, the only curative treatment for high-risk or refractory hematologic malignancies non-responsive to standard chemotherapy is allogeneic hematopoietic transplantation (allo-HCT). Acute graft-versus-host disease (GVHD) is a donor T cell-mediated immunological disorder that is frequently fatal...

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Autores principales: Neidemire-Colley, Lotus, Robert, Jérémy, Ackaoui, Antoine, Dorrance, Adrienne M., Guimond, Martin, Ranganathan, Parvathi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9727380/
https://www.ncbi.nlm.nih.gov/pubmed/36505438
http://dx.doi.org/10.3389/fimmu.2022.1033490
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author Neidemire-Colley, Lotus
Robert, Jérémy
Ackaoui, Antoine
Dorrance, Adrienne M.
Guimond, Martin
Ranganathan, Parvathi
author_facet Neidemire-Colley, Lotus
Robert, Jérémy
Ackaoui, Antoine
Dorrance, Adrienne M.
Guimond, Martin
Ranganathan, Parvathi
author_sort Neidemire-Colley, Lotus
collection PubMed
description To date, the only curative treatment for high-risk or refractory hematologic malignancies non-responsive to standard chemotherapy is allogeneic hematopoietic transplantation (allo-HCT). Acute graft-versus-host disease (GVHD) is a donor T cell-mediated immunological disorder that is frequently fatal and the leading cause of non-relapse mortality (NRM) in patients post allo-HCT. The pathogenesis of acute GVHD involves recognition of minor and/or major HLA mismatched host antigens by donor T cells followed by expansion, migration and finally end-organ damage due to combination of inflammatory cytokine secretion and direct cytotoxic effects. The endothelium is a thin layer of endothelial cells (EC) that line the innermost portion of the blood vessels and a key regulator in vascular homeostasis and inflammatory responses. Endothelial cells are activated by a wide range of inflammatory mediators including bacterial products, contents released from dying/apoptotic cells and cytokines and respond by secreting cytokines/chemokines that facilitate the recruitment of innate and adaptive immune cells to the site of inflammation. Endothelial cells can also be damaged prior to transplant as well as by alloreactive donor T cells. Prolonged EC activation results in dysfunction that plays a role in multiple post-transplant complications including but not limited to veno-occlusive disease (VOD), transplant associated thrombotic microangiopathy (TA-TMA), and idiopathic pneumonia syndrome. In this mini review, we summarize the biology of endothelial cells, factors regulating EC activation and the role of ECs in inflammation and GVHD pathogenesis.
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spelling pubmed-97273802022-12-08 Role of endothelial cells in graft-versus-host disease Neidemire-Colley, Lotus Robert, Jérémy Ackaoui, Antoine Dorrance, Adrienne M. Guimond, Martin Ranganathan, Parvathi Front Immunol Immunology To date, the only curative treatment for high-risk or refractory hematologic malignancies non-responsive to standard chemotherapy is allogeneic hematopoietic transplantation (allo-HCT). Acute graft-versus-host disease (GVHD) is a donor T cell-mediated immunological disorder that is frequently fatal and the leading cause of non-relapse mortality (NRM) in patients post allo-HCT. The pathogenesis of acute GVHD involves recognition of minor and/or major HLA mismatched host antigens by donor T cells followed by expansion, migration and finally end-organ damage due to combination of inflammatory cytokine secretion and direct cytotoxic effects. The endothelium is a thin layer of endothelial cells (EC) that line the innermost portion of the blood vessels and a key regulator in vascular homeostasis and inflammatory responses. Endothelial cells are activated by a wide range of inflammatory mediators including bacterial products, contents released from dying/apoptotic cells and cytokines and respond by secreting cytokines/chemokines that facilitate the recruitment of innate and adaptive immune cells to the site of inflammation. Endothelial cells can also be damaged prior to transplant as well as by alloreactive donor T cells. Prolonged EC activation results in dysfunction that plays a role in multiple post-transplant complications including but not limited to veno-occlusive disease (VOD), transplant associated thrombotic microangiopathy (TA-TMA), and idiopathic pneumonia syndrome. In this mini review, we summarize the biology of endothelial cells, factors regulating EC activation and the role of ECs in inflammation and GVHD pathogenesis. Frontiers Media S.A. 2022-11-23 /pmc/articles/PMC9727380/ /pubmed/36505438 http://dx.doi.org/10.3389/fimmu.2022.1033490 Text en Copyright © 2022 Neidemire-Colley, Robert, Ackaoui, Dorrance, Guimond and Ranganathan https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Neidemire-Colley, Lotus
Robert, Jérémy
Ackaoui, Antoine
Dorrance, Adrienne M.
Guimond, Martin
Ranganathan, Parvathi
Role of endothelial cells in graft-versus-host disease
title Role of endothelial cells in graft-versus-host disease
title_full Role of endothelial cells in graft-versus-host disease
title_fullStr Role of endothelial cells in graft-versus-host disease
title_full_unstemmed Role of endothelial cells in graft-versus-host disease
title_short Role of endothelial cells in graft-versus-host disease
title_sort role of endothelial cells in graft-versus-host disease
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9727380/
https://www.ncbi.nlm.nih.gov/pubmed/36505438
http://dx.doi.org/10.3389/fimmu.2022.1033490
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