Epithelial HMGB1 Delays Skin Wound Healing and Drives Tumor Initiation by Priming Neutrophils for NET Formation

Esther Hoste, Christian Maueröder, Lisette van Hove, Leen Catrysse, Hanna Kaisa Vikkula, Mozes Sze, Bastiaan Maes, Dyah Karjosukarso, Liesbet Martens, Amanda Gonçalves, Eef Parthoens, Ria Roelandt, Wim Declercq, Ignacia Fuentes, Francis Palisson, Sergio Gonzalez, Julio C. Salas-Alanis, Louis Boon, Peter Huebener, Klaas Willem MulderKodi Ravichandran, Yvan Saeys, Robert Felix Schwabe, Geert van Loo

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

Inflammation mediates tissue repair but can be hijacked to promote tumorigenesis. Hoste et al. demonstrate that HMGB1 delays regeneration and drives tumor formation in skin by recruitment and priming of neutrophils. These data indicate that therapies targeting HMGB1 or NET formation might be relevant in chronic and diabetic wound treatment.

Original languageEnglish
Pages (from-to)2689-2701.e4
JournalCell Reports
Volume29
Issue number9
DOIs
StatePublished - Nov 26 2019

Keywords

  • diabetes
  • epidermolysis bullosa
  • HMGB1
  • innate immunity
  • neutrophil extracellular traps
  • skin inflammation
  • TNF
  • tumor microenvironment
  • wound healing

Fingerprint

Dive into the research topics of 'Epithelial HMGB1 Delays Skin Wound Healing and Drives Tumor Initiation by Priming Neutrophils for NET Formation'. Together they form a unique fingerprint.

Cite this