Passage of immune complexes through vascular walls. Evidence for the role of an immediate hypersensitivity mechanism and its mediator: platelet-activating factor.

An anaphylactic mechanism involving IgE-sensitized basophils is necessary for immune complex deposition in rabbits. Basophils under stimulation by the IgE-bound antigen actively release a platelet-activating factor. Increased vascular permeability results from action of vasoactive amines from basophils and from aggregated platelets and possibly direct action of PAF on vascular walls. This allows trapping of circulating complexes along vascular membranes. Once deposited complexes produce tissue injury by neutrophil-complement-dependent mechanisms. However, complex deposition seems pathogenic in itself for the glomerular basement membrane. PAF is a 1,100-dalton MW lipid, with hydrophobic properties and positive charge; it exists in human basophils. Patients suffering from SLE or undergoing anaphylactic shocks exhibit marked reduction of basophil counts and PAF level. We propose that anaphylactic increase of vasopermeability may be a common feature at early stages of many immune diseases associated with severe structural injury.