FIGURE 18-3 Pathologic features of antibody-mediated glomerulonephritis. A, Glomerulonephritis induced by an antibody against the glomerular basement membrane (Goodpasture's syndrome): the light micrograph shows glomerular inflammation and severe damage, and immunofluorescence shows smooth (linear) deposits of antibody along the basement membrane. B, Glomerulonephritis induced by the deposition of immune complexes (systemic lupus erythematosus): the light micrograph shows neutrophilic inflammation, and the immunofluorescence and electron micrograph show coarse (granular) deposits of antigen-antibody complexes along the basement membrane. (Immunofluorescence micrographs are courtesy of Dr. Jean Olson, Department of Pathology, University of California, San Francisco, and the electron micrograph is courtesy of Dr. Helmut Rennke, Department of Pathology, Brigham and Women's Hospital, Boston Massachusetts.)
serum not containing the antitoxin, so the lesions could not be attributed to the anti-diphtheria antibody. Second, the symptoms appeared at least a week after the first injection of horse serum and more rapidly with each repeated injection. von Pirquet concluded that this disease was due to a host response to some component of the serum. He suggested that the host made antibodies to horse serum proteins, these antibodies formed complexes with the injected proteins, and the disease was due to the antibodies or immune complexes. We now know that his conclusions were entirely accurate. He called this disease serum disease; it is now more commonly known as serum sickness and is the prototype for systemic immune complex-mediated disorders.
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