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Published on: October 21, 2013
[Phagocytic activity of monocytes tin glomerulonephritis in complete remission]
Insights
Phagocytic activity of monocytes is reduced in active glomerulonephritis (GN), impairing the removal of immune complexes. This defect is not seen in GN remission, suggesting it’s linked to active disease, not serum inhibitors.
Area of Science:
- Nephrology
- Immunology
- Cell Biology
Context:
- Circulating immune complexes (CIC) are a primary cause of glomerulonephritis (GN).
- Phagocyte activity is crucial for clearing CIC, but its role in GN pathogenesis is not fully understood.
Purpose:
- To investigate the phagocytic function of peripheral monocytes in patients with active GN and those in remission.
- To determine if reduced phagocytic activity contributes to CIC accumulation in GN.
Summary:
- Phagocytic activity, measured by phagocytic index and percentage, was significantly decreased in monocytes from patients with active GN (membranous GN, membranoproliferative GN, lipoid nephrosis) compared to controls.
- This phagocytic defect was not observed in patients with GN in complete remission and was independent of serum factors, suggesting an intrinsic monocyte dysfunction.
- The findings indicate that impaired monocyte phagocytosis in active GN may lead to insufficient clearance of CIC.
Impact:
- Highlights a potential mechanism contributing to GN progression and severity.
- Suggests that assessing monocyte phagocytic function could aid in diagnosing and managing GN.
- Opens avenues for therapeutic strategies targeting phagocyte function in GN treatment.
Abstract:
Circulating immune complexes (CIC) account for a majority of GN. Their pathogenicity depends on size, molecular composition, glomerular hemodynamics and activity of phagocytes. The phagocytic function of peripheral monocytes was studied in 23 patients with non-systemic active GN and in 16 GN in complete remission. Phagocytic activity of peripheral blood monocytes was assessed in vitro, by calculating phagocytic index (IP: number of zymozan particles in each monocyte) and phagocytosis percentage (PP: number of phagocyting monocytes); the tests were carried out on autologous and heterologous serum samples. In 13 controls, PP was 79 +/- 5.8%. In 7 membranous GN, 6 membranoproliferative GN and 10 lipoid nephrosis, PP was severely decreased, 63.4 +/- 9.6%, 52.1 +/- 19% and 52.2 +/- 14%. In each group of GN, these results were significantly different from controls (p less than 0.01). In all groups these results were similar in autologous and heterologous serum samples (55 +/- 13% and 57.5 +/- 16%; NS). This perturbation was not observed in GN in complete remission. Therefore, this defect was not linked to the presence of serum inhibitors. In conclusion, alterations of phagocytic activity is present in some primary active GN and may explain an insufficient rate of CIC removal.
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