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Inhibition of complement-dependent lymphocyte rosette formation by sera of patients with chronic glomerulonephritis
Insights
Activated complement C3 products can inhibit lymphocyte rosette formation. This assay effectively detects activated complement components in patients with chronic glomerulonephritis and lupus erythematosus.
Area of Science:
- Immunology
- Nephrology
- Complement System
Background:
- Activated complement C3 products can bind to lymphocyte C3 receptors.
- This binding may inhibit complement-dependent lymphocyte rosette formation.
Purpose of the Study:
- To evaluate the utility of a complement-dependent rosette inhibition assay.
- To detect activated complement components in patients with chronic glomerulonephritis (GN) and systemic lupus erythematosus (SLE).
Main Methods:
- Sera from GN and SLE patients were tested using a complement-dependent rosette inhibition assay.
- Normal donor lymphocytes served as reacting cells.
- Control groups included healthy donors and patients with other diseases.
Main Results:
- Sera from most membranoproliferative GN and SLE patients significantly inhibited rosette formation.
- Two-thirds of focal glomerulosclerosis patients' sera were inhibitory.
- Inhibitory activity correlated with low serum C3 levels, but could occur with normal C3 levels.
- No correlation was found between patient's rosette count and serum inhibitory activity.
Conclusions:
- The complement-dependent rosette inhibition assay is a valuable tool.
- It can be routinely used to detect free or immune complex-bound activated complement components.
- This assay aids in diagnosing and monitoring GN and SLE patients.
Abstract:
It has been demonstrated that activated C3 products might bind to lymphocyte C3 receptors and inhibit subsequent complement-dependent lymphocyte rosette formation. Sera from patients with various types of chronic glomerulonephritis (GN) have been tested in a complement-dependent rosette inhibition assay using normal donors' lymphocytes as reacting cells. Control subjects consisted of healthy donors and patients with miscellaneous renal and general diseases. Most sera of membranoproliferative GN and of systemic lupus erythematosus, and two-thirds sera of focal glomerolosclerosis patients, significantly inhibited rosette formation. Only 15-40 percent sera of patients with other types of GN were inhibitory. Serum inhibiting activity usually correlated with low serum C3 level (P less than 0.0005), although inhibition could be observed with normal serum C3. However, no correlation was found between a patient's own complement-dependent lymphocyte rosette count and his serum inhibitory activity. These results extend previous findings and suggest that the complement-dependent rosette inhibition assay can be used routinely to detect serum activated complement components either free or bound to immune complexes.