Modulation of CR1 transcript in systemic lupus erythematosus (SLE) by IFN-gamma and immune complex

Mol Immunol. 2007 Mar;44(7):1722-8. doi: 10.1016/j.molimm.2006.07.300. Epub 2006 Oct 16.


Reduced expression of Erythrocyte Complement Receptor 1 (E-CR1) is envisaged to contribute significantly to the pathophysiology of systemic lupus erythematosus (SLE). We determined the levels of CR1 transcript in the neutrophils from 25 untreated patients with active SLE and 25 normal healthy individuals and, studied the effect of interferon-gamma (IFN-gamma), interleukin-4 (IL-4) and immune complexes (IC) on the same. The study revealed a marked decline in the levels of neutrophil CR1 (N-CR1) transcript in the patients with SLE, and differential pattern of IFN-gamma and IL-4 expression in the neutrophils from normals and patients. Opsonized immune complexes down regulated CR1 transcript in patients and IFN-gamma up regulated the same both in normals and patients. Immune complexes suppressed this effect of IFN-gamma. IL-4 also suppressed the effect of IFN-gamma but effect confined only to the normals. This is the first real-time RT-PCR data comparing the neutrophil CR1 expression in normals and patients with SLE and its modulation by IFN-gamma, IL-4 and immune complexes. IFN-gamma and immune complexes, respectively, emerged as the positive and negative modulators of neutrophil CR1 transcript in SLE.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antigen-Antibody Complex / pharmacology
  • Female
  • Humans
  • Interferon-gamma / genetics
  • Interferon-gamma / metabolism*
  • Interferon-gamma / pharmacology
  • Interleukin-4 / genetics
  • Interleukin-4 / metabolism
  • Interleukin-4 / pharmacology
  • Lupus Erythematosus, Systemic / genetics
  • Lupus Erythematosus, Systemic / immunology*
  • Male
  • Neutrophils / chemistry
  • Neutrophils / drug effects
  • Neutrophils / immunology*
  • RNA, Messenger / analysis
  • RNA, Messenger / metabolism
  • Receptors, Complement 3b / analysis
  • Receptors, Complement 3b / genetics*
  • Receptors, Complement 3b / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transcription, Genetic / drug effects


  • Antigen-Antibody Complex
  • RNA, Messenger
  • Receptors, Complement 3b
  • Interleukin-4
  • Interferon-gamma