Anti-
lamin B autoantibodies are associated with both
systemic lupus erythematosus (SLE) and autoimmune
liver disease. We examined the possibility that the underlying clinical feature in patients with anti-
lamin B autoantibodies might be chronic autoimmune
liver disease, and whether the
hypergammaglobulinemia present in both disorders is involved in generating anti-
lamin B autoantibodies. A
lamin B fusion
protein (MLB1), consisting of
amino acids 77-533 of
lamin B fused to TrpE, was used to screen sera from 84 patients with SLE for anti-
lamin B autoantibodies. 3/4 prototype human
lamin B antisera, 5/84 SLE sera (6%), and 0/30 sera from healthy individuals reacted with MLB1 on immunoblots at a 1:500 dilution. Of the 9 anti-
lamin B autoantibody positive patients studied, all but 1 fulfilled at least four ARA criteria for SLE. None of the patients displayed evidence of chronic autoimmune
liver disease, suggesting that autoimmune
liver disease is not strongly associated with anti-
lamin B antibodies in SLE. In SLE, as in "lupoid
hepatitis", anti-
lamin B autoantibodies are often produced transiently during periods of increased disease activity. Although polyclonal
hypergammaglobulinemia is also associated with increased activity of both diseases, anti-
lamin B autoantibody production in 2 patients was independent of total
immunoglobulin levels,
antibodies to irrelevant
proteins, and production of some other
autoantibodies. Thus, polyclonal activation is insufficient to explain either the initiation or regulation of anti-
lamin B autoantibody production, supporting the hypothesis that
antinuclear antibodies are
antigen-selective.