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Research Article Free access | 10.1172/JCI107700
1Arthritis and Clinical Immunology Unit, Monroe Community Hospital, and the Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642
Find articles by Wagner, T. in: JCI | PubMed | Google Scholar
1Arthritis and Clinical Immunology Unit, Monroe Community Hospital, and the Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642
Find articles by Abraham, G. in: JCI | PubMed | Google Scholar
1Arthritis and Clinical Immunology Unit, Monroe Community Hospital, and the Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642
Find articles by Baum, J. in: JCI | PubMed | Google Scholar
Published June 1, 1974 - More info
The induction of chemotactic factor by rheumatoid factor (RF) and by rheumatoid complexes and their constituents was investigated. The presence of chemotactic factor was measured by the number of polymorphonuclear leukocytes (obtained from normal individuals) attracted through a 3 μm Millipore filter and is expressed as a “chemotactic index.” The chemotactic index was used to measure the effect of immunoglobulins and their complexes in stimulating production of complement-derived chemotactic factors from the sera of normal individuals.
Two sources of IgG (F-II and DEAE-purified IgG) were used. These were prepared for use in the native and heat-aggregated states. The same chemotactic index was obtained with both these preparations of IgG. The chemotactic index increases when (a) increasing concentrations of gamma globulin were added to a constant concentration of complement and (b) when the amount of complement alone was increased.
The addition of a purified IgM RF to the mixture of IgG and complement caused a decrease in the chemotactic index. Incubation of IgG and complement before addition of IgM RF produced no change in the chemotactic index. The addition of a nonrheumatoid factor IgM to IgM and complement had no effect on the chemotactic index. IgM RF and IgG alone were not chemotactic.
These studies confirm the concept of “complement deviation” by IgM RF which occurs with, and as a result of, the immune complex formation between IgG and IgM RF. The successful activation of complement chemotactic factors by IgG may explain the synovitis with high polymorphonuclear leukocyte counts found in RF-negative arthritis.