The current status of targeting BAFF/BLyS for autoimmune diseases

Arthritis Res Ther. 2004;6(5):197-202. doi: 10.1186/ar1222. Epub 2004 Jul 29.


It is increasingly recognized that B cells have multiple functions that contribute to the pathogenesis of autoimmunity. Specific targeting of B cells might therefore be an appropriate therapeutic intervention. The tumor necrosis factor-like molecule BAFF (BLyS) is a key B cell survival factor and its receptors are expressed on most peripheral B cells. Several different BAFF antagonists are under development and in early clinical trials. We review here the rationale for BAFF blockade, and its predicted mechanism of action in autoimmune diseases.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Autoimmune Diseases / drug therapy*
  • B-Cell Activating Factor
  • Humans
  • Membrane Proteins / antagonists & inhibitors*
  • Receptors, Tumor Necrosis Factor / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*


  • B-Cell Activating Factor
  • Membrane Proteins
  • Receptors, Tumor Necrosis Factor
  • TNFSF13B protein, human
  • Tumor Necrosis Factor-alpha