Abstract.New Zealand Black (NZB) mice spontaneously develop Coombs positive autoimmune hemolytic anemia. The pathogenesis of the hemolytic anemia was investigated through radioisotopic methods using chromium‐labeled (51Cr) syngeneic erythrocytes to measure the chromium disappearance rate. Chromium disappearance was monitored in both the presence and absence of ‘bound’ autoantibodies. Technetium‐labeled colloidal sulfide (99mTc) was injected i.v. to assess the phagocytic activity of the reticuloendothelial system. The mean rate of disappearance of chromium from the circulation of Coombs negative NZB mice was comparable to that of a control CBA strain. Coombs positive NZB mice had a greater destruction rate with the rate being proportional to the degree of autoantibody sensitization. The hepatic technetium uptake in Coombs positive NZB mice was about 50% greater than in Coombs negative NZB mice. The spleen and bone marrow had a greater uptake and the liver a smaller uptake of99mTc in Coombs negative NZB mice than in a control group of mice.It is concluded that both erythrocyte autoantibodies and increased reticuloendothelial activity influence the destruction of erythrocytes in Coombs positive N
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