Article Text
PDFNew targets
Is NF-κB a useful therapeutic target in rheumatoid arthritis?
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
Statistics from Altmetric.com
- 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