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Complement activation induces the expression of decay-accelerating factor on human mesangial cells.
T Shibata1, F G Cosio, D J Birmingham
1Department of Internal Medicine and Pathology, Ohio State University, Columbus 43210.
Journal of Immunology (Baltimore, Md. : 1950)
|December 1, 1991
Summary
Immune complex activation of complement on mesangial cells increases decay-accelerating factor (DAF) synthesis and expression. This DAF may protect kidney cells from complement-mediated damage during glomerulonephritis.
Area of Science:
- Immunology
- Nephrology
- Cell Biology
Background:
- Immune complexes (IC) and complement activation are implicated in glomerulonephritis.
- The role of decay-accelerating factor (DAF) in protecting glomerular cells is not fully understood.
Purpose of the Study:
- To investigate the effect of complement activation by IC on DAF expression in human mesangial cells (MC).
- To determine the mechanism of DAF induction and its characteristics on MC.
Main Methods:
- MC were cultured and incubated with antigens and antibodies to form IC.
- Complement activation was induced using human serum.
- DAF expression was measured by immunoperoxidase staining and RIA.
- DAF biophysical properties and function were analyzed.
Main Results:
- IC formation and complement activation significantly increased DAF expression on MC plasma membrane.
- DAF induction was dependent on terminal complement components (C5b-9).
- Increased DAF expression resulted from de novo synthesis by MC, confirmed by cycloheximide and actinomycin D experiments.
- MC DAF exhibited properties similar to DAF in other cells, including resistance to trypsin, pronase sensitivity, and phosphatidylinositol anchor.
Conclusions:
- Deposition of terminal complement components on human MC triggers DAF synthesis and membrane expression.
- DAF may protect glomerular cells from complement-mediated injury in immune complex-mediated glomerulonephritis.