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The apoptosis-1/Fas protein in human systemic lupus erythematosus

E Mysler1, P Bini, J Drappa

  • 1Hospital for Special Surgery, Cornell University Medical Center, New York 10021.

The Journal of Clinical Investigation
|March 1, 1994
PubMed

Insights

Systemic lupus erythematosus (SLE) patients show higher APO-1/Fas receptor expression on lymphocytes, but no functional defect was found in this apoptosis pathway in vitro.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • Mutations in the APO-1/Fas receptor pathway cause lupus-like disease in mice.
  • Investigating the role of this apoptosis pathway in human Systemic Lupus Erythematosus (SLE) is crucial.

Purpose of the Study:

  • To determine if humans with SLE have defects in the APO-1/Fas mediated apoptosis pathway.
  • To analyze APO-1 receptor expression and function on lymphocytes from SLE patients.

Main Methods:

  • Flow cytometry and anti-APO-1 antibody were used to analyze APO-1 expression on freshly isolated and in vitro activated blood mononuclear cells.
  • Analysis included peripheral B cells, CD4+ and CD8+ T lymphocytes.
  • Apoptosis induction by anti-APO-1 antibody was assessed in activated SLE and normal lymphocytes.

Main Results:

  • Significantly higher APO-1 expression was observed on freshly isolated B cells and T lymphocytes from SLE patients compared to controls (P < 0.001).
  • APO-1 upregulation was linked to in vivo lymphocyte activation, as indicated by co-expression with CD29.
  • No defects in APO-1 regulation or function (apoptosis induction) were detected in vitro in activated SLE lymphocytes.

Conclusions:

  • While APO-1/Fas signaling is important for lymphocyte survival in SLE, this study found no consistent defect in receptor expression or function in vitro.
  • Further research is needed to fully elucidate the role of the APO-1/Fas pathway in SLE pathogenesis.

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