Polyclonal B-cell activation of autoantibodies in ( CBA N × NZB)F₁ mice by polyinosinic polycytidylic acid

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.