Systemic lupus erythematosus: a blissless disease of too much BLyS (B lymphocyte stimulator) protein

Curr Opin Rheumatol. 2002 Sep;14(5):522-8. doi: 10.1097/00002281-200209000-00007.

Abstract

B lymphocyte stimulator (BLyS) protein is among the novel tumor necrosis factor (TNF) ligands and receptor superfamily members recently described. BLyS protein can promote B cell survival, expansion, and differentiation both and. Constitutive overexpression of BLyS protein can result in systemic lupus erythematosus (SLE)-like disease in mice, and circulating levels of BLyS protein are elevated in a subset of human SLE patients. Treatment of SLE mice with a BLyS protein antagonist ameliorates disease progression and enhances survival. By inference, BLyS protein may also play an important contributory role in pathogenesis and/or propagation of human SLE and becomes a legitimate candidate target for antagonist biologic agents.

Publication types

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

MeSH terms

  • Animals
  • B-Cell Activation Factor Receptor
  • B-Lymphocytes / metabolism
  • Disease Models, Animal
  • Humans
  • Lupus Erythematosus, Systemic / immunology
  • Lupus Erythematosus, Systemic / metabolism*
  • Membrane Proteins*
  • Mice
  • Mice, Transgenic
  • Neuropeptides / metabolism
  • Nuclear Proteins / metabolism
  • Receptors, Tumor Necrosis Factor / antagonists & inhibitors
  • Receptors, Tumor Necrosis Factor / biosynthesis*
  • Receptors, Tumor Necrosis Factor / immunology
  • Receptors, Tumor Necrosis Factor / metabolism

Substances

  • ANP32B protein, human
  • B-Cell Activation Factor Receptor
  • BLyS receptor
  • Membrane Proteins
  • Neuropeptides
  • Nuclear Proteins
  • Receptors, Tumor Necrosis Factor
  • TNFRSF13C protein, human
  • Tnfrsf13c protein, mouse