Abstract
Abstract The development of autoimmunity in New Zealand mice is related to genetic, immunologic and viral factors. Evidence was presented to suggest that thymus-dependent immune functions may be depressed and bone marrow-dependent functions augmented in these mice. Antibodies to RNA and DNA appear spontaneously and can also be induced by treatment with polyinosinic·polycytidylic acid (rI·rC). Antibodies binding 14C-rI·rC in human lupus sera and in New Zealand mice developing lupus have greatest specificity for reovirus double-stranded RNA. Treatment of New Zealand mice with RNA and cyclophosphamide induces immunologic tolerance and suppresses antibodies binding 14C-rI·rC. Induction of tolerance in this way prevents the accelerated formation of anti-RNA antibodies normally induced by Moloney leukemia virus. This finding suggests that virus-accelerated and natural disease occur through a similar mechanism, and supports the hypothesis that common viruses may act as an antigenic stimuli for a genetically hyper-responsive antibody-producing system.
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