THE INTERACTION OF IMMUNE COMPLEXES WITH RBC AND PHAGOCYTIC CELLS (RED BLOOD CELLS, COMPLEMENT, ANTIBODY, ERYTHROCYTES, MONOCYTE, ANTIGEN)

In our studies, we started by examining the interaction of surface-bound immune complexes (IC) with PMN leukocytes, placing particular emphasis on the release of platelet activating factor (PAF). Having proved that insoluble and immobilized soluble IC trigger the release of PAF from PMN leukocytes and that insoluble IC stimulate interleukin 1 (IL 1) release from monocytes, we proceeded to study whether IC adsorbed to human erythrocytes (RBC) would induce the same effects. Having concluded that such was the case, we studied the conditions that surround RBC-IC interactions as well as the fate of RBC-bound IC and of the RBC themselves after interaction with phagocytic cells.;In Chapter II we describe our studies concerning immune complex binding to RBC. We initially observed that heat aggregated gamma globulin bound readily to HRBC, even under conditions excluding complement mediated activity. In addition, soluble IC (particularly when prepared at antigen excess) were capable of binding to HRBC in vitro in absence of complement. Further investigations determined that the antigens (tetanus toxoid and hemocyanin) used in the preparation of soluble IC at antigen excess were themselves capable of in vitro adsorption to HRBC.;In Chapter III we describe our studies on the interaction of soluble TT-ATT IC adsorbed onto HRBC with PMN leukocytes and monocytes. Our studies were focused on: (1) the fate of IC and (2) the fate of the red cells themselves.;Another set of experiments was designed to study the activation capacity of IC-HRBC interactions with PMN or monocytes, measuring the release of PAF and IL 1, respectively. (Abstract shortened with permission of author.).;Chapter I describes our studies of the interactions between soluble tetanus toxoid-rabbit antitetanus toxoid (TT-ATT) IC, insoluble TT-ATT IC, and surface-bound IC with PMN leukocytes in which the in vitro release of PAF was the principal activation parameter measured. Our results indicated that insoluble IC and surface bound IC stimulated substantial PAF release from PMN leukocytes; in contrast, soluble IC proved to be very poor stimuli of PAF release.