Induction of erythrocyte autoantibodies in NZB mice: spectrotype and relationship with the Xid gene.

The production of autoantibodies to erythrocytes by immunization with rat red blood cells (RRBC) is significantly retarded in X-linked immune deficient (Xid) mice. We have attempted to further explore this relationship by characterizing RRBC-induced erythrocyte autoantibodies in high responder New Zealand Black (NZB) and congenic NZB.Xid mice. NZB.Xid animals, immunized with RRBC, readily produce anti-RRBC antibodies and cross-reactive antiautologous erythrocyte antibody (CR anti-MRBC) as well as anti-HB antibodies. The autoantibody response of NZB.Xid mice to RRBC appears similar to NZB controls with respect to both the time of onset and subclass diversity; the anti-HB antibody cannot be absorbed with RRBC. Moreover, there are no alterations in the spectrotype of antierythrocyte antibodies found in NZB.Xid mice. Nonetheless, NZB.Xid, but not NZB mice, fail to produce splenic plaque-forming responses against bromelase-treated mouse red blood cells. Lyb 5+ cells are not required for the production of RRBC-induced antierythrocyte autoantibodies. These results, when discussed in light of the low but significant incidence of spontaneous DAT in NZB.Xid mice, suggest that given the appropriate genetic repertoire, the influence of the Xid gene on autoantibody production can be bypassed.