You are here

  • Home
  • Archive
  • Volume 78, Issue 2
  • REDD1/autophagy pathway promotes thromboinflammation and fibrosis in human systemic lupus erythematosus (SLE) through NETs decorated with tissue factor (TF) and interleukin-17A (IL-17A)

Article info

Article menu

Download PDFPDF

Systemic lupus erythematosus
REDD1/autophagy pathway promotes thromboinflammation and fibrosis in human systemic lupus erythematosus (SLE) through NETs decorated with tissue factor (TF) and interleukin-17A (IL-17A)

Authors

  • Eleni Frangou Laboratory of Immune Regulation and Tolerance, Autoimmunity and Inflammation, Biomedical Research Foundation of the Academy of Athens, Athens, Greece Department of Internal Medicine, Medical School, University of Cyprus, Nicosia, Cyprus Department of Nephrology and Transplantation, Nicosia General Hospital, Nicosia, Cyprus PubMed articlesGoogle scholar articles
  • Akrivi Chrysanthopoulou Department of Internal Medicine, Laboratory of Molecular Hematology, Democritus University of Thrace, Alexandroupolis, Greece PubMed articlesGoogle scholar articles
  • Alexandros Mitsios Department of Internal Medicine, Laboratory of Molecular Hematology, Democritus University of Thrace, Alexandroupolis, Greece PubMed articlesGoogle scholar articles
  • Konstantinos Kambas Department of Internal Medicine, Laboratory of Molecular Hematology, Democritus University of Thrace, Alexandroupolis, Greece PubMed articlesGoogle scholar articles
  • Stella Arelaki Department of Pathology, University Hospital of Alexandroupolis, Democritus University of Thrace, Alexandroupolis, Greece PubMed articlesGoogle scholar articles
  • Iliana Angelidou Department of Internal Medicine, Laboratory of Molecular Hematology, Democritus University of Thrace, Alexandroupolis, Greece PubMed articlesGoogle scholar articles
  • Athanasios Arampatzioglou Department of Internal Medicine, Laboratory of Molecular Hematology, Democritus University of Thrace, Alexandroupolis, Greece PubMed articlesGoogle scholar articles
  • Hariklia Gakiopoulou 1st Department of Pathology, National and Kapodistrian University of Athens Medical School, Athens, Greece PubMed articlesGoogle scholar articles
  • George K Bertsias Rheumatology, Clinical Immunology and Allergy, University of Crete School of Medicine, Heraklion, Greece PubMed articlesGoogle scholar articles
  • Panayotis Verginis Laboratory of Immune Regulation and Tolerance, Autoimmunity and Inflammation, Biomedical Research Foundation of the Academy of Athens, Athens, Greece PubMed articlesGoogle scholar articles
  • Konstantinos Ritis Department of Internal Medicine, Laboratory of Molecular Hematology, Democritus University of Thrace, Alexandroupolis, Greece First Department of Internal Medicine, University Hospital of Alexandroupolis, Democritus University of Thrace, Alexandroupolis, Greece PubMed articlesGoogle scholar articles
  • Dimitrios T Boumpas Laboratory of Immune Regulation and Tolerance, Autoimmunity and Inflammation, Biomedical Research Foundation of the Academy of Athens, Athens, Greece Department of Internal Medicine, Medical School, University of Cyprus, Nicosia, Cyprus 4th Department of Medicine, Attikon University Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece PubMed articlesGoogle scholar articles
  1. Correspondence to Dr Dimitrios T Boumpas, Attikon University Hospital, 1 Rimini str, Haidari 1264, Athens, Greece; boumpasd{at}uoc.gr
View Full Text

Citation

Frangou E, Chrysanthopoulou A, Mitsios A, et al
REDD1/autophagy pathway promotes thromboinflammation and fibrosis in human systemic lupus erythematosus (SLE) through NETs decorated with tissue factor (TF) and interleukin-17A (IL-17A)
Annals of the Rheumatic Diseases 2019;78:238-248.

Publication history

  • Received February 4, 2018
  • Revised October 28, 2018
  • Accepted November 1, 2018
  • First published December 18, 2018.
Online issue publication 
August 02, 2019

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Copyright information

© Author(s) (or their employer(s)) 2018. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.