Abstract
Assuming that anti-allotypic anti-Ig in rheumatoid arthritis is stimulated by the individual's allotype, it would be reasonable to expect a higher incidence of anti-G1m(a) in individuals carrying G1m(a). There is marked divergence among various populations in allotype frequencies. G1m(a) allotype and the prevalence of anti-Ig reactive with G1m(a) Ig were determined in 18 Kuwaiti, 23 Japanese, and 41 Swedish rheumatoid arthritis patients. An inverse relationship was observed between the frequency distribution of allotype G1m(a) and anti-allotype; thus, the stimulus for the anti-allotype is not the patient's own allotype.
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