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Interleukin-21 receptor deficiency increases the initial toll-like receptor 2 response but protects against joint pathology by reducing Th1 and Th17 cells during streptococcal cell wall arthritis.

Authors
  • Marijnissen, Renoud J
  • Roeleveld, Debbie M
  • Young, Deborah
  • Nickerson-Nutter, Cheryl
  • Abdollahi-Roodsaz, Shahla
  • Garcia de Aquino, Sabrina
  • van de Loo, Fons A J
  • van Spriel, Annemiek B
  • Boots, Annemieke M H
  • van den Berg, Wim B
  • Koenders, Marije I
Type
Published Article
Journal
Arthritis & rheumatology (Hoboken, N.J.)
Publication Date
Apr 01, 2014
Volume
66
Issue
4
Pages
886–895
Identifiers
DOI: 10.1002/art.38312
PMID: 24757141
Source
Medline
License
Unknown

Abstract

In contrast to the proinflammatory role of IL-21 in adaptive immunity, which drives IL-17+IFN+ cells and joint pathology during chronic experimental arthritis, IL-21 also has an important immunosuppressive role, presumably by inhibiting TLR signaling via SOCS-1 and SOCS-3. If this dual role of IL-21 in various immune processes is present in human disease, it could make IL-21 a difficult therapeutic target in rheumatoid arthritis.

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