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The persistence of interleukin-6 is regulated by a blood buffer system derived from dendritic cells

Authors
  • Yousif, Ashraf S.1
  • Ronsard, Larance1
  • Shah, Pankaj2
  • Omatsu, Tatsushi2
  • Sangesland, Maya1
  • Bracamonte Moreno, Thalia1
  • Lam, Evan C.1
  • Vrbanac, Vladimir D.1
  • Balazs, Alejandro B.1
  • Reinecker, Hans-Christian2, 3
  • Lingwood, Daniel1
  • 1 The Ragon Institute of Massachusetts General Hospital, The Massachusetts Institute of Technology and Harvard University, 400 Technology Square, Cambridge, MA 02139, USA
  • 2 The Center for the Study of Inflammatory Bowel Disease, Center for Computational and Integrative Biology, Massachusetts General Hospital, 185 Cambridge Street, Boston, MA 02114, USA
  • 3 The Center for the Genetics of Host Defense, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390, USA
Type
Published Article
Journal
Immunity
Publication Date
Dec 22, 2020
Volume
54
Issue
2
Pages
235–246
Identifiers
DOI: 10.1016/j.immuni.2020.12.001
PMID: 33357409
PMCID: PMC7836640
Source
PubMed Central
Keywords
License
Unknown

Abstract

Hyper-elevated IL-6 underscores cytokine storming and chronic inflammatory disorders. Yousif et al. demonstrate that conventional dendritic cells are a major source of sIL-6R, which forms a buffer system that sets the in-solution persistence of IL-6, regulating inflammatory immune reactions.

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