Although the etiology of rheumatic diseases has not been elucidated, it seems to be involved in excessive autoimmune responses. In 1976, we began to research rheumatic diseases, especially rheumatoid arthritis. Anti-human immunoglobulin allotype antibodies in Japanese sera were collected from blood donors or patients by hemagglutination and the hemagglutination inhibition method using anti-D sensitized erythrocytes. Many rheumatoid factors without any specificity to IgG allotypes (Gm allotypes) were detected in patient sera. On the other hand, so-called anti-antibodies, Andresen type but not Milgrom type, were mainly detected in blood donors. Thirty-nine sera possessing anti-Gm and anti-Km antibody specificities were finally obtained by screening about 80,000 Japanese. The antibody to G1m (f) was most frequently detected, but the antibody to G1m (z), which is an allele of G1m (f), was not obtained. Quantitative evaluation of rheumatoid factors (RF) and anti-citrullinated protein antibodies (ACPA) was adopted in the 2010 ACR/EULAR classification criteria for rheumatoid arthritis; however, quality management of RF has been incompletely implemented in Japan. We therefore mounted an effort to standardize the cutoff value. We found marked hyperferritinemia in patients with active adult Still's disease in 1987. Additionally, ratios of glycosylated ferritin in the patients were extremely reduced, even if they came into the inactive phase. This depressive production of glycosylated ferritin might be a marked characteristic of this disease. Finally, the development of musculoskeletal ultrasonography in rheumatic diseases is introduced.

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