CBA N × NZB F1 male mice, which fail to produce a primary antibody response to rI·rC, were capable of responding to multiple injections of rI·rC with an IgG antibody response. Such antibody was made only after 4-5 months of treatment with rI·rC which was markedly delayed in comparison with NZB × CBA N F1 males and CBA N × NZB F1 females. In addition, CBA N × NZB F1 males responded to rI·rC injection with anti-DNA production. LPS was somewhat less effective than rI·rC with regard to autoantibody stimulation. Treatment with rI·rC reduced survival in these crosses by 50% in comparison with untreated mice. However, the X-linked immune defect in serum IgM concentrations in ( CBA N × NZB)F1 male mice was maintained. Thus, the presence of the X-linked defect in ( CBA N × NZB)F1 male mice did not provide protection from stimulation of autoantibody production by prolonged administration of a polyclonal B-cell activator.
ASJC Scopus subject areas
- Immunology and Allergy
- Pathology and Forensic Medicine