The release of IgE-dependent platelet-activating factor (PAF) from basophils and the deposition of immune complexes (IC) in glomeruli were studied in 76 rabbits injected i.v. with a large amount of bovine serum albumin (BSA). The results demonstrated that glomerulonephritis and proteinuria occurred only in 43 rabbits in which in vivo degranulation of basophils occurred during the early stage of serum sickness and in which in vitro sensitization of basophils to BSA was detected after the immune clearance of BSA. An additional group of rabbits was preimmunized to horseradish peroxidase (HRP), and 20 animals were selected on the basis of high titers of IgE anti-HRP antibodies and a high degree of in vitro basophil degranulation to HRP. These 20 rabbits were then injected with BSA to evaluate the basophil sensitization to HRP during the course of the acute serum sickness. Twelve of these 20 rabbits developed glomerulonephritis and showed 1) basophil desensitization to HRP; 2) decreased amounts of PAF releasable from basophils and from renal tissue; 3) platelet desensitization to PAF; and 4) detectable intravascular release of PAF in 5 rabbits. The kinetic study of the glomerular immune deposits showed that the first appearance of immune deposits in antigen excess was preceeded by in vivo basophil degranulation. In the later stages of serum sickness, the immune deposits showed a progressive increase in rabbit IgG and C3. Our results are consistent with the interpretation that the IgE-dependent release of PAF from basophils contributes to increasing vascular permeability, thus favoring the deposition of circulating IC in glomerular structures during the initial stage of experimentally induced acute serum sickness.
|Number of pages||9|
|Journal||Journal of Immunology|
|Publication status||Published - 1982|
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