Extracellular Vesicles as Mediators of Cellular Crosstalk Between Immune System and Kidney Graft.
Cytokines
/ metabolism
Endothelial Cells
/ metabolism
Extracellular Vesicles
/ immunology
Immune System
/ immunology
Kidney
/ immunology
Kidney Diseases
Kidney Transplantation
Kidney Tubules
/ metabolism
Macrophages
/ metabolism
Mesenchymal Stem Cells
/ metabolism
Reperfusion Injury
/ immunology
T-Lymphocytes
/ immunology
Transplants
/ immunology
acute rejection
autoimmunity
biomarker
extracellular vesicles
ischemia-reperfusion syndrome
miRNA
renal transplant
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2020
2020
Historique:
received:
06
11
2019
accepted:
13
01
2020
entrez:
18
3
2020
pubmed:
18
3
2020
medline:
4
3
2021
Statut:
epublish
Résumé
Extracellular vesicles (EVs) are known immune-modulators exerting a critical role in kidney transplantation (KT). EV bioactive cargo includes graft antigens, costimulatory/inhibitory molecules, cytokines, growth factors, and functional microRNAs (miRNAs) that may modulate expression of recipient cell genes. As paracrine factors, neutrophil- and macrophage-derived EVs exert immunosuppressive and immune-stimulating effects on dendritic cells, respectively. Dendritic cell-derived EVs mediate alloantigen spreading and modulate antigen presentation to T lymphocytes. At systemic level, EVs exert pleiotropic effects on complement and coagulation. Depending on their biogenesis, they can amplify complement activation or shed complement inhibitors and prevent cell lysis. Likewise, endothelial- and platelet-derived EVs can exert procoagulant/prothrombotic effects and also promote endothelial survival and angiogenesis after ischemic injury. Kidney endothelial- and tubular-derived EVs play a key role in ischemia-reperfusion injury (IRI) and during the healing process; additionally, they can trigger rejection by inducing both alloimmune and autoimmune responses. Endothelial EVs have procoagulant/pro-inflammatory effects and can release sequestered self-antigens, generating a tissue-specific autoimmunity. Renal tubule-derived EVs shuttle pro-fibrotic mediators (TGF-β and miR-21) to interstitial fibroblasts and modulate neutrophil and T-lymphocyte influx. These processes can lead to peritubular capillary rarefaction and interstitial fibrosis-tubular atrophy. Different EVs, including those from mesenchymal stromal cells (MSCs), have been employed as a therapeutic tool in experimental models of rejection and IRI. These particles protect tubular and endothelial cells (by inhibition of apoptosis and inflammation-fibrogenesis or by inducing autophagy) and stimulate tissue regeneration (by triggering angiogenesis, cell proliferation, and migration). Finally, urinary and serum EVs represent potential biomarkers for delayed graft function (DGF) and acute rejection. In conclusion, EVs sustain an intricate crosstalk between graft tissue and innate/adaptive immune systems. EVs play a major role in allorecognition, IRI, autoimmunity, and alloimmunity and are promising as biomarkers and therapeutic tools in KT.
Identifiants
pubmed: 32180768
doi: 10.3389/fimmu.2020.00074
pmc: PMC7057849
doi:
Substances chimiques
Cytokines
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
74Informations de copyright
Copyright © 2020 Quaglia, Dellepiane, Guglielmetti, Merlotti, Castellano and Cantaluppi.
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