A B S T R A C Texhibit Rh specificity and did not react with nonprimate red cells. When studied by sucrose gradient ultracentrifugation, the vG antibodies to human red cells in these eluates sedimented in the 7S region. It is concluded that in many patients in whom direct antiglobulin tests reveal only cell-bound complement, the complement fixation is mediated in vivo by small quantities of "warmreacting" erythrocyte autoantibodies of the aG class.
In vivo-formed antigen-antibody complexes cause transient glomerulonephritis and vasculitis in experimental animals when appropriate antigens are administered to unimmunized animals in a single dose (1, 2). Similar antigens administered in multiple doses induce chronic disease (1, 3). Antigen, antibodies, and complement components have been demonstrated in lesions produced in this manner. Furthermore, antigen-antibody complexes have been shown as causative agents of glomerulonephritis in human systemic lupus erythematosus (4), acute poststreptococcal glomerulonephritis (5), malaria (6), and other conditions. However, in experimental models and in human diseases, the characteristics of immune complexes that become entrapped by vascular and glomerular basement membranes to cause disease are not fully understood. In addition, detailed descriptions are not available on the characteristics of immune complexes that form in vivo from the native antibodies and the antigens that are introduced experimentally in animals or by disease processes in man. Similarly, quantitative information on the fate of such complexes is lacking.When antigens are administered to immunized animals in small doses or if immune complexes are given to nonimmunized animals, the immune complexes are removed rapidly in part by the reticuloendothelial system (7, 8). Weigle (9) showed that if intravenously injected antigen-antibody complexes are prepared at equivalence or in slight antigen excess, they are quickly removed from the circulation of rabbits and that similar complexes prepared in large antigen excess persist longer. He concluded that the size of the complexes played a major role in their clearance from the circulation. Cochrane and Hawkins (10) also indicated that immune complexes greater than 19S are quickly removed from the circulation of guinea pigs and that small antigen-antibody complexes persist in the circulation. These investigators suggested that the immune complexes had to exceed a certain critical size and that vascular permeability had to be increased before complexes were entrapped by vascular or glomerular basement membranes. The half-life of the complexes that are rapidly removed has not been well defined and the role of the complement-fixing ability of these complexes has not been characterized fully.
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