1989 年 8 巻 3 号 p. 353-360
The etiology of rheumatoid arthritis (RA) is debatable and remains obscure. However, it is generally agreed that the disease develops in a genetically predisporsed individual with the aid of some unidentified environmental factor, such as a viral infection, acting as a precipitating cause.
We surmise that an alteration in the properties of complement activation inhibitory factors could result in inflammatory reactions against homologous cells and contribute to causing an autoimmune disease.
Based on this hypothesis, we investigated the decay accelerating factor (DAF), an inhibitory factor of C3 convertases, in peripheral blood mononuclear cells of RA patients. The cells of 28 RA patients and 12 healthy volunteers were subjected to an FACS analysis using indirect immunofluorescence with the anti-DAF monoclonal antibody (IC6) .
The results showed that an average of only 34.7% of the peripheral blood mononuclear cells of RA patients were positive for surface DAF compared to a corresponding value for healthy subjects of 63.3%.
