Dickkopf proteins in pathological inflammatory diseases

Min Hee Park, Jae Hun Shin, Alfred L.M. Bothwell, Wook Jin Chae

Research output: Contribution to journalReview articlepeer-review

Abstract

The human body encounters various challenges. Tissue repair and regeneration processes are augmented after tissue injury to reinstate tissue homeostasis. The Wnt pathway plays a crucial role in tissue repair since it induces target genes required for cell proliferation and differentiation. Since tissue injury causes inflammatory immune responses, it has become increasingly clear that the Wnt ligands can function as immunomodulators while critical for tissue homeostasis. The Wnt pathway and Wnt ligands have been studied extensively in cancer biology and developmental biology. While the Wnt ligands are being studied actively, how the Wnt antagonists and their regulatory mechanisms can modulate immune responses during chronic pathological inflammation remain elusive. This review summarizes DKK family proteins as immunomodulators, aiming to provide an overarching picture for tissue injury and repair. To this end, we first review the Wnt pathway components and DKK family proteins. Next, we will review DKK family proteins (DKK1, 2, and 3) as a new class of immunomodulatory protein in cancer and other chronic inflammatory diseases. Taken together, DKK family proteins and their immunomodulatory functions in chronic inflammatory disorders provide novel insights to understand immune diseases and make them attractive molecular targets for therapeutic intervention.

Original languageEnglish (US)
Pages (from-to)893-901
Number of pages9
JournalJournal of Leukocyte Biology
Volume111
Issue number4
DOIs
StatePublished - Apr 2022
Externally publishedYes

Keywords

  • Wnt
  • antagonist
  • cancer
  • immunology

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology

Fingerprint

Dive into the research topics of 'Dickkopf proteins in pathological inflammatory diseases'. Together they form a unique fingerprint.

Cite this