Nephrol Dial Transplant (2001) 16: 1764-1768
© 2001 European Renal Association-European Dialysis and Transplant Association
Invited Comment
Nuclear factor 
B for the nephrologist
Note added in proof In murine macrophages Connelly et al. have clarified that early release of NO upregulates NF
B, whilst later NO downregulates NFB. Connelly M, Palacios-Callender M, Ameixa C, Moncada S, Hobbs AJ. Biphasic regulation of NF-B activity underlies the pro- and antiinflammatory actions of nitric oxide. J Immunol 2001; 166: 3873–3881.
North Leigh, Oxon, UK
Introduction
Nuclear factor kappa B (NFB) is a rapid response transcription factor that works to ensure survival of all cells that might be subjected to environmental stress, injury, inflammation or immune reactions. NFB activation leads to control of genes for the expression of cytokines and chemokines, immunoreceptors, cell adhesion molecules, growth factors or acute phase proteins. Thus, directly or indirectly, NFB controls a wide variety of biological responses, in particular those that are part of innate and adaptive immunity. Cellular expression of NFB is constitutive in B and T lymphocytes, in monocytes and neurones, or it is inducible in other cells.
NFB structure and function
NFB was discovered by Sen and Baltimore (1986) in mature B cells as a nuclear transcription factor, which binds to an element in the -immunoglobin light chain enhancer. Soon it was found that NFB occurs in most cells as an active cytoplasmic form, consisting
Upstream activation of the IB kinase complex
Measuring NFB
Pathophysiological activation of NFB
Inflammation: glomerulonephritides
Proteinuria and tubulo-interstitial injury
Angiotensin II and vascular damage
Ischaemia-reperfusion injury
Infections
Diabetes-related pathophysiology
Alcoholism
Dehydration: renal papillary damage
Notes
References