The morphology and the kinetics of an inflammatory reaction elicited by immune complexes was investigated and the role of complement in the reaction was ascertained. The hallmark of the direct active (DAA) and reversed passive (RPA) Arthus reactions was the accumulation of immune precipitates and polymorphonuclear leukocytes (PMN) in and around vessels. Using fluoresceinated antigen as a tracer, immune complexes were localized in the lumina and walls of venules and small veins in the DAA and in the wall of vessels and perivascularly in RPA. PMN accumulated at these same sites, phagocytosed the fluoresceinated complexes and became degranulated. The precise localization of immune complexes was achieved by examining the same tissue sections 1st by fluorescence microscopy, followed by conventional staining and examination by light microscopy. Marked stasis of the microcirculation was observed, particularly in DAA, in which a few immune complex-containing PMN were entrapped in a mass of densely packed red blood cells. Some edema was observed in early lesions and definitive separation of collagen fibers was noted in lesions older than 2 h. Hemorrhage became the dominant characteristic of both types of reactions from 2 h onward. By administering radiolabeled cells, proteins and microspheres as a pulse, given at various times before sacrifice, the quantitation and kinetics of the inflammatory lesions elicited by immune complexes was elucidated. In RPA all parameters quantitated reached a peak soon after elicitation of the reaction (2-4 h). In DAA there was some difficulty in assessing the quantitation because of interanimal variations and because of progression of the inflammatory lesions, as the antigen diffused peripherally from the site of its injection. Peak activities occurred in 4- to 8-h-old lesions. These observations and a comparison of the center and periphery of the lesions, strengthened the contention that the RPA and DAA have common features and features which differ. In common were immunological mechanisms (antigen-antibody interaction and complement activation) and cellular events (polymorphonuclear leukocyte chemotaxis, phagocytosis and release of lysosomal contents). Different features were the site of immune complex formation and its sequela. In RPA they formed primarily in the wall of venules and small veins and hence had a marked effect on increase in vessel permeability. In the DAA most of the complexes formed and the leukocytes accumulated in the lumen of the same vessels. These events were reflected in microcirculatory blood flow. In RPA most intense hyperemia was seen in the center of a lesion, whereas in DAA, because of the occlusive immune complexes and associated intravascular leukocyte and platelet accumulations, blood flow in the center gradually diminished. However, hyperemia continued at the periphery as antigen diffused centrifugally. In rabbits rendered hypocomplementemic PMN accumulation was markedly reduced and as a consequence increase in vessel permeability was abrogated and hemorrhage markedly suppressed. In contrast to other forms of acute inflammation, inflammation induced by immune complexes is entirely host-mediated and the kinetics of the immune complex-initiated inflammatory reaction, at least in RPA, is similar to reactions initiated by other particulate or soluble stimuli.