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Radiolabelled staphylococcal protein A was used to quantitate the binding of IgG on stored human platelets from human sera containing specific antibodies reactive with platelets and rabbit serum containing immune complexes (IC). Normal human serum (NHS) inhibited the binding of IC onto platelets and to various extents also the binding of specific antibodies. The attachment of inhibitors to platelets seemed to be reversible. The considerable difference in the inhibitory capacities of IgG-deficient sera and monomeric IgG indicates that IgG is the major inhibitory component of NHS. The binding of IgG from NHS onto platelets evidently hampers the detection of weak platelet antibodies even with the most sensitive tests. Purified Clq, known lo modify the reactions of IC with fresh platelets did not alter the binding of IC onto stored platelets. A monoclonal, antiglobulin-active rheumatoid factor of IgM class displayed only moderate inhibition. Therefore, the application of RF or Clq for the differentiation of the binding induced by IC or antibodies is not useful in this assay system. The heterogeneity of immunologic receptors of platelets provides an explanation of the inhibitory inefficiency of Clq. [ABSTRACT FROM AUTHOR]

Model experiments with preformed antigen-antibody complexes have shown that the platelet aggregation test can be used to characterize immune complexes. The platelet aggregating activity of four sera behaved like antigen-antibody complexes -with respect to the effect of added antigen, added antibody and sedimentation in density gradient centrifugation. Two of the sera were from patients with fever of unknown origin. The findings suggest that the two sera contained circulating immune complexes which had both measles hyperimmunization induced and normal specificities. The serum of a patient with fatal subacute hepatitis seemed to contain immune complexes with Australia antigen. It was also positive in many of the autoimmunity tests. One of the sera was from a patient with haemorrhagic varicella in the acute phase of the disease. The patient had received large amounts of y-globulin. The results suggested the transient presence of circulating immune complexes with varicella specificity. [ABSTRACT FROM AUTHOR]

Hepatitis and other sera were studied for direct platelet aggregating (P1.A.) activity in non-heated and heat-treated state, for inhibitability of P1.A. by antiglobulin active cryoglobulin IgM components (Cryo-IgM), and for sedimentation velocity of P1.A. activity by sucrose gradient centrifugation. Three distinct patterns of direct P1.A. activity were established: (1) 'aggregated IgG type': heating-dependent, ≧ 9S, inhibitable by Cryo-IgM, serum anticomplementary; (2) 'antibody type': heating-independent, 7S and/or 19S, non-inhibitable by Cryo-IgM, serum not anticomplementary; and (3) 'immune-complex type': heating-independent, ≧19S, inhibitable by Cryo-lgM, anticomplementary activity present or absent. In the heavy P1.A.-active sucrose gradient serum fractions of one patient, only IgG4 Gm markers were detected. [ABSTRACT FROM AUTHOR]

Aggregation of human platelets (P1.A) induced by IgG immune complexes of rabbit (Ea-aEa, NIP2-24 BSA-aNIP) and human (tetanus toxoid-aT) origin and by heat-aggregated human polyclonal IgG was inhibitable by antiglobulin-active IgM components dissociated from IgM-IgG cryoglobulins. The inhibitory capacity of the Cryo-IgM components extended over a wide range of Ag:Ab ratios on both sides of the equivalence, and likewise over a wide range of epitope densities on the Ag portion of the P1.A active Ag--Ab complex. In contrast to the inhibitability of IgG complex-induced P1.A was the total lack of inhibition by Cryo-IgM components of P1.A induced by anti-platelet rabbit antibodies. The P1.A active IgG complexes inhibitable by Cryo-IgM were shown by sucrose gradient centrifugation analyses to be greater than 19S. This type of complexes was also present in a number of patient sera. It is concluded that the application of antiglobulin-active cryoglobulin IgM components in combination with the P1.A phenomenon provide a useful means for detection and analysis of circulating complexes and for differentiation of complex-induced P1.A from antibody-induced P1.A. [ABSTRACT FROM AUTHOR]

The article focuses on interaction between human blood platelets, viruses and antibodies. Post-infectious thrombocytopenic purpura seems to be a clinical entity and distinct from other haemorrhagic complications of virus diseases. The thrombocytopenic purpura in Rubella develops abruptly during the 1st week after the rash, and usually disappears within a few weeks, but it may last for months. An increased destruction of circulating platelels seems to be the most important pathogenic mechanism in post-infectious thrombocytopenia. Injury to platelets may be caused by a direct effect of virus on platelets or by some immunological mechanism.