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IL-32γ and streptococcus pyogenes cell wall fragments synergise for IL-1-dependent destructive arthritis via upregulation of TLR-2 and NOD2
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  1. B Heinhuis1,
  2. M I Koenders1,
  3. F A van de Loo1,
  4. P L E M van Lent1,
  5. S-H Kim3,
  6. C A Dinarello3,
  7. L A B Joosten2,
  8. W B van den Berg1
  1. 1Rheumatology Research and Advanced Therapeutics, Department of Rheumatology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
  2. 2Department of Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
  3. 3Division of Infectious Diseases, University of Colorado, Denver, Colorado, USA

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Purpose

Interleukin 32 (IL-32) might play an important role in the pathogenesis of RA by inducing cytokines and chemokines. IL-32 is highly expressed in RA synovial tissue and strongly correlates with synovial inflammation, tumour necrosis factor (TNF)α and IL-1 expression. IL-32 alone is not that potent, but it appears to enhance sensitivity of synovial cells to proinflammatory stimuli. Here, we investigated potential synergistic effects …

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