B cell receptor signaling in human systemic lupus erythematosus

Curr Opin Rheumatol. 2006 Sep;18(5):451-5. doi: 10.1097/01.bor.0000240353.99808.5f.


Purpose of review: The purpose of this review is to inform the scientific community of the most recent findings surrounding B cell receptor signaling function in human systemic lupus erythematosus and how altered B cell signaling may explain the characteristic hyperactivity of B cells in active disease and contribute to its pathogenesis.

Recent findings: B cell receptor signaling is abnormal in patients with active systemic lupus erythematosus as demonstrated by increased calcium flux and global B cell hyperactivity. Altered signaling has been explained by a variety of factors such as defective FcgammaRIIB signaling, decreased expression of the protein tyrosine kinase Lyn, and increased serum levels of B lymphocyte stimulator.

Summary: The studies reviewed suggest that B cells from systemic lupus erythematosus patients display molecular signaling defects that most likely contribute to pathogenesis of the disease and explain the characteristic hyperactivity of B cells in active disease.

Publication types

  • Review

MeSH terms

  • Antigens, CD / genetics
  • Antigens, CD / immunology
  • B-Lymphocytes / immunology*
  • B-Lymphocytes / pathology
  • Humans
  • Interleukin-1 / immunology
  • Lupus Erythematosus, Systemic / genetics
  • Lupus Erythematosus, Systemic / immunology*
  • Lupus Erythematosus, Systemic / pathology
  • Lymphocyte Activation / genetics
  • Lymphocyte Activation / immunology*
  • Receptors, Antigen, B-Cell / genetics
  • Receptors, Antigen, B-Cell / immunology*
  • Receptors, IgG / genetics
  • Receptors, IgG / immunology
  • Signal Transduction / genetics
  • Signal Transduction / immunology*
  • src-Family Kinases / genetics
  • src-Family Kinases / immunology


  • Antigens, CD
  • Fc gamma receptor IIB
  • Interleukin-1
  • Receptors, Antigen, B-Cell
  • Receptors, IgG
  • lyn protein-tyrosine kinase
  • src-Family Kinases