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Migration inhibition factor in acute serum sickness nephritis
G Parra1, J Mosquera, B Rodríguez-Iturbe
1Renal Service and Laboratory, Hospital Universitario de Maracaibo, Venezuela.
Kidney International
|December 1, 1990
Summary
Monocytes are key in acute serum sickness nephritis. Glomerular migration inhibition factor (MIF) production correlates with lymphocyte and monocyte accumulation, suggesting a role in kidney inflammation.
Area of Science:
- Nephrology
- Immunology
- Pathology
Background:
- Monocytes play a critical role in acute serum sickness (AcSS) nephritis.
- Local lymphokine production may drive monocyte accumulation in glomeruli.
Purpose of the Study:
- Investigate migration inhibition factor (MIF) activity in glomerular cultures.
- Analyze the temporal relationship between MIF, monocyte, and lymphocyte accumulation.
- Assess the impact of anti-T lymphocyte monoclonal antibody on local MIF production.
Main Methods:
- AcSS induced in rabbits; kidneys harvested at 4 and 14 days post-antigen elimination.
- Lymphocytes identified by M108 antibody; monocytes by non-specific esterase stain (ES).
- MIF activity measured using the agarose microdroplet method in glomerular culture supernatants.
Main Results:
- Peak MIF activity (84.3%) coincided with peak lymphocyte (1.15/gcs) and monocyte (2.4 ES score/gcs) infiltration on day 1 of proteinuria.
- MIF activity decreased to 66.0% by day 4 and 12.8% by day 14.
- Significant correlations found between lymphocyte infiltration and MIF (r=0.776) and MIF and monocyte accumulation (r=0.858).
Conclusions:
- MIF production in glomeruli is closely linked to lymphocyte and monocyte infiltration during AcSS nephritis.
- These findings highlight the role of local lymphokine production in driving inflammatory cell accumulation in the glomerulus.