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Is NF-κB a useful therapeutic target in rheumatoid arthritis?
  1. M Feldmann,
  2. E Andreakos,
  3. C Smith,
  4. J Bondeson,
  5. S Yoshimura,
  6. S Kiriakidis,
  7. C Monaco,
  8. C Gasparini,
  9. S Sacre,
  10. A Lundberg,
  11. E Paleolog,
  12. N J Horwood,
  13. F M Brennan,
  14. B M J Foxwell
  1. Kennedy Institute of Rheumatology Division, Faculty of Medicine, Charing Cross Hospital Campus, Arthritis Research Campaign Building, 1 Aspenlea Road, London W6 8LH, UK
  1. Correspondence to:
    Professor M Feldmann;
    m.feldmann{at}ic.ac.uk

Abstract

There is increasing evidence that NF-κB is a major, if not the major transcription factor regulating inflammation and immunity. While this implies that blocking NF-κB might be therapeutically beneficial, it raises clear questions regarding the balance between efficacy and safety. In this brief review we discuss the effects of NF-κB blockade in rheumatoid arthritis, inflammation and immunity, and consider possible therapeutic targets within the NF-κB family.

  • rheumatoid arthritis
  • nuclear factor κB
  • APC, antigen presenting cell
  • DC, dendritic cells
  • ELISA, enzyme linked immunosorbent assay
  • GM-CSF, granulocyte macrophage colony stimulating factor
  • IKK2, IκB kinase 2
  • IL, interleukin
  • LPS, lipopolysaccharide
  • MHC, major histocompatibility complex
  • MMP, matrix metalloproteinase
  • m.o.i., multiplicity of infection
  • PBS, phosphate buffered saline
  • PSI, proteosome inhibitor
  • RA, rheumatoid arthritis
  • [3H]TdR, [3H]thymidine
  • TIMP, tissue inhibitor of matrix metalloproteinase
  • TNFα, tumour necrosis factor α

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