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A role of complement receptors on polymorphonuclear leukocytes in the adherence to immune deposit
Abstract:
Polymorphonuclear leukocytes (PMNs) adhered tightly to glomeruli with immune complex in vitro in the cryostat sections of nephritic kidneys. The sections were incubated with PMNs for 40 min at 37 degrees C. The kidneys were obtained from rats with experimental glomerulonephritis induced by the prolonged administration of bovine serum albumin. This PMN adherence occurred when PMNs were suspended in fresh rat serum (one-step method) or the sections were treated with the fresh serum prior to the incubation with PMNs (two-step method). However, this adherence was inhibited by treatment of PMNs with trypsin to destroy their complement receptors. The inhibition was concomitant with the decrease in the percentage of rosette-formation by complement-coated zymosan particles. In addition, the adherence was markedly suppressed in both methods using decomplemented serum with zymosan. The aggregated rabbit gammaglobulin opsonized with fresh serum also inhibited the binding of PMNs to the glomeruli by the occupation of the complement receptors on PMNs. These findings indicated the important role of complement components on the glomeruli with immune deposits and complement receptors on PMNs in the PMN adherence.
Insights
Polymorphonuclear leukocytes (PMNs) bind to kidney glomeruli in glomerulonephritis. This adherence relies on complement receptors on PMNs and complement components within immune deposits.
Area of Science:
- Nephrology
- Immunology
- Cell Biology
Background:
- Glomerulonephritis involves immune complex deposition in kidney glomeruli.
- Polymorphonuclear leukocytes (PMNs) are key inflammatory cells implicated in kidney damage.
Purpose of the Study:
- To investigate the mechanism of PMN adherence to glomeruli in experimental glomerulonephritis.
- To elucidate the role of complement system components and receptors in this adherence process.
Main Methods:
- In vitro incubation of cryostat kidney sections from rats with experimental glomerulonephritis with PMNs.
- Utilizing one-step and two-step methods involving fresh or decomplemented rat serum.
- Assessing adherence inhibition through PMN treatment with trypsin and using complement-coated zymosan particles or opsonized aggregated rabbit gammaglobulin.
Main Results:
- PMNs adhered to glomeruli containing immune complexes.
- Adherence was dependent on complement receptors on PMNs and complement components on glomeruli.
- Trypsin treatment of PMNs or use of decomplemented serum significantly inhibited adherence.
- Opsonized aggregated rabbit gammaglobulin also blocked PMN binding.
Conclusions:
- Complement components on glomerular immune deposits and complement receptors on PMNs are crucial for PMN adherence in glomerulonephritis.
- Understanding this interaction is vital for developing targeted therapies for kidney diseases.