Surface and functional characteristics of B cells from lupus-prone murine strains

B lymphocyte hyperactivity in systemic lupus erythematosus (SLE)-prone mice, originall considered a result of imbalances in T-cell subsets, more recently has been attributed to intrinsic abnormalities of B cells. In our experiments cited here, we used a variety of systems to assess the surface phenotypic and functional characteristics of B cells from several SLE strains (NZB, NZB/W, BXSB, MRL/Mp-lpr/lpr). Generation of Ig isotype diversity follows normal pathways in all these SLE strains. B cells from newborn BXSB and MRL/Mp-lpr/lpr mice, as in immunologically normal mice, do not reexpress surface Ig (sIg) after modulation with anti-Ig. In contrast, B cells of newborn New Zealand mice do reexpress sIg after anti-Ig-induced modulation. The rates at which sIg-anti-Ig complexes cap and become endocytosed in all SLE strains are within normal limits. B cells from SLE strains are stimulated mitogenically by F(ab') 2 anti-μ and lipopolysaccharide with indices no different from those of normal B cells. The ontogenic development of Ia + and Lyb5 + cells is normal with the frequency of positive cells and density of alloantigens normal or slightly elevated, respectively. SLE and normal strains are much alike in expression of retroviral envelope gp70 antigen on surfaces of lymphocytes. Anti-gp70 antibodies fail to stimulate mitosis in cells of either SLE or normal strains. However, the frequency of B-cell colony-forming splenocytes is several fold higher in autoimmune mice compared to controls. Expression of acceptor sites for helper messages and of acceptor sites for suppressor messages on B cells is within normal limits in all SLE mice as revealed by the effects of immune response enhancing anti-Lyb3 serum and immune response suppressing anti-Lyb7 serum, respectively. As a whole, these results reaffirm the generalized hyperactivity and advanced maturation of B cells of SLE mice but do not reveal any common surface or functional characteristics which might be responsible for the B-cell abnormality.