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Ribosomal P antibodies and CNS lupus.

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  • 1Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA. morris-reichlin@omrf.ouhsc.edu

Lupus
|January 13, 2004
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Summary
This summary is machine-generated.

Autoantibodies to ribosomal P proteins (anti-P) are linked to central nervous system (CNS) disease in systemic lupus erythematosus (SLE) patients. Evidence suggests anti-P antibodies may directly contribute to psychosis and other CNS manifestations in SLE.

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Area of Science:

  • Immunology
  • Neurology
  • Rheumatology

Background:

  • Autoantibodies to ribosomal P proteins (anti-P) are recognized in systemic lupus erythematosus (SLE).
  • An early association between anti-P antibodies and psychosis in SLE patients was observed.
  • The precise role of anti-P antibodies in central nervous system (CNS) disease remains a subject of investigation.

Purpose of the Study:

  • To review and synthesize the evidence linking anti-P antibodies to CNS disease in SLE.
  • To explore the potential mechanisms by which anti-P antibodies may contribute to CNS manifestations.
  • To discuss the relationship between anti-P antibodies and other autoantibodies in SLE-related CNS disease.

Main Methods:

  • Review of independent studies investigating the association between anti-P antibodies and CNS disease.
  • Analysis of longitudinal data correlating anti-P antibody fluctuations with psychosis episodes.
  • Examination of studies on the correlation of anti-P antibodies with general SLE disease activity.
  • Investigation of anti-P antibody presence and activity in lupus renal tissue eluates.
  • Assessment of evidence for P protein accessibility on cells and the effects of anti-P antibodies on cellular protein synthesis.

Main Results:

  • Seven independent studies demonstrate a strong association between anti-P antibodies and CNS disease in SLE.
  • Longitudinal studies show anti-P antibody levels fluctuate with psychosis episodes.
  • Anti-P antibodies correlate with overall SLE disease activity.
  • Acid eluates from lupus renal tissue show a 30-fold enrichment of anti-P antibody activity, suggesting a direct role.
  • Evidence indicates P protein is accessible on normal cells, and anti-P antibodies can enter cells, inhibiting protein synthesis.

Conclusions:

  • Substantial evidence links anti-P antibodies to various forms of CNS disease in SLE patients.
  • Anti-P antibodies may play a direct role in the pathogenesis of SLE-related CNS manifestations, including psychosis.
  • Other autoantibodies, such as anti-dsDNA and antiglial fibrillary protein, may also contribute to CNS disease in SLE.
  • Further research is needed to clarify the relative contributions of different autoantibodies to CNS disease in SLE.