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Prostaglandin E2 modulation of rheumatoid factor synthesis.
A Alvarellos1, P E Lipsky, H E Jasin
1Harold C. Simmons Arthritis Research Center, University of Texas Southwestern Medical Center, Dallas 75235-9030.
Arthritis and Rheumatism
|December 1, 1988
Summary
Prostaglandin E2 (PGE2) significantly inhibits rheumatoid factor (RF) production by B cells, especially when their surface immunoglobulin is cross-linked. This points to a potential regulatory defect in rheumatoid arthritis.
Area of Science:
- Immunology
- Rheumatology
- Cell Biology
Background:
- Rheumatoid factor (RF) is a key autoantibody in rheumatoid arthritis.
- The regulation of RF synthesis by immune cells is not fully understood.
Purpose of the Study:
- To investigate the role of prostaglandin E2 (PGE2) in regulating in vitro rheumatoid factor (RF) synthesis.
- To explore the mechanisms by which PGE2 influences B and T lymphocyte function.
Main Methods:
- Purified human B and T lymphocytes were stimulated with Staphylococcus aureus Cowan 1 or pokeweed mitogen (PWM).
- Prostaglandin E2 (PGE2) and heat-aggregated IgG (HAIgG) were added to assess their effects on RF and IgM secretion.
- Lymphocytes from rheumatoid arthritis patients were analyzed.
Main Results:
- PGE2 significantly inhibited RF and IgM secretion induced by S. aureus Cowan 1.
- PGE2's inhibition of RF was more pronounced than IgM inhibition, particularly at lower concentrations.
- Adding HAIgG enhanced PGE2-mediated inhibition of RF synthesis in PWM-stimulated cultures.
- PGE2-mediated suppression was independent of T helper cell activity.
- Lymphocytes from rheumatoid arthritis patients showed impaired sensitivity to PGE2-mediated inhibition.
Conclusions:
- Down-regulation of RF synthesis requires both surface immunoglobulin cross-linking and PGE2 influence.
- Defects in this immunoregulatory pathway may contribute to persistent RF production in rheumatoid arthritis.