Ontogenesis of RBC autoantibody response

Early work showed that neonatal thymectomy of NZB mice failed to prevent the generation of RBC autoantibody, although thymectomy immediately after birth appeared to delay the onset of autoantibody production. It was also established that RBC autoantibody production can be transferred to irradiated non-NZB H-2d recipients with bone marrow cells. Since the anti-RBC plaque-forming response still occurred in chronically T-depleted recipients, it was argued that an intrinsic defect was present in NZB B cells and implied that the RBC autoantibody response was T-independent. Recent work calls these interpretations into question. First, SCID mice repopulated with NZB pre-B cells fail to develop RBC autoantibodies despite that fact that high levels of IgM anti-DNA and low levels of IgG anti-DNA are generated. Secondly, chronic treatment of NZB mice with monoclonal anti-CD4 prevents or considerably delays the generation of RBC autoantibodies. Interestingly, anemia still occurs in anti-CD4-treated NZB mice, possibly because they developed an ulcerative colitis. Finally, Gershwin and his colleagues have generated CD4 and CD8 gene-deleted NZB mice. Again the incidence and titers of RBC autoantibodies (particularly of the IgM isotype) were significantly reduced in NZB.CD4~/_ mice as compared with wild-type NZBs. By contrast, no significant change in RBC autoantibody responses was observed in NZB.CD8" ' mice. Thus CD4 T cells clearly contribute to the development of NZB AIHA.

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