Interaction of Human IgM Rheumatoid Factors with Immune Complexes in Experimental Murine Glomerulonephritis

Abstract

The occurrence of circulating IgM antiglobulin (rheumatoid factor) has been noted in a number of human diseases other than rheumatoid arthritis, in which immune complexes (IC’s) are felt to have a pathogenetic role. These diseases include bacterial endocarditis, several forms of glomerulonephritis, systemic lupus, vasculitis and cryoglobulinemia. In all these diseases rheumatoid factor (RF) occurs not only in the circulation, but has been identified at the site of the damaged tissue. Furthermore RF has been identified as a component of cryoprecipitable IC’s in cryoglobulinemia [1]. It has been known for many years that RF is capable of reacting with IC’s in vitro [2] and this capacity forms the basis of one group of methods for the laboratory measurement of IC levels in body fluids [3], More recently there has been interest in the role of RF’s in human glomerulonephritis. Rossen et al. [4] noted the presence of RF in the glomeruli of patients with chronic glomerulonephritis associated with IC’s and observed that RF was more likely to be found in severe than in mild disease. Mcintosh et al. [5] identified RF in the blood of patients with poststreptococcal infection as soon as 7 or 8 days after the initial streptococcal infection and at the time of the onset of the renal damage and also demonstrated RF in the glomeruli of a patient with acute glomerulonephritis [6]. In patients with essential mixed cryoglobulinemia and renal involvement the RF component of the cryo has also been identified in the glomerulus [7].