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Polyanion-immunoglobulin complexes, considered important factors in the pathogenesis of glomerulonephritis common in systemic lupus erythematosus, were found and isolated from sera of NZB mice by selectively binding them to an anion-exchange cellulose (DE52). Accurate quantification of such complexes was possible, in terms of immunoglobulin content, by means of an antiglobulin complement-fixation assay. In sera of NZB mice the concentration of immune complexes increased up to about 11 months of age and then it declined, whereas in the sera of the C57B1 and HaICR strains of mice, which do not develop spontaneous glomerulonephritis, the concentration was lower initially but increased steadily with increasing age and reached an equivalent level at about 27 months. The complexes were composed primarily of immunoglobulins of the IgG class bound to native DNA. The finding of significant levels of circulating immune complexes in mouse strains without renal disease suggests that such complexes, although necessary, might not be sufficient and solely responsible for overt glomerulonephritis. [ABSTRACT FROM AUTHOR]

An antigen recognized by antisera produced against p30 (core) proteins of the four chief groups of mammalian type C viruses (murine, feline, RD-114 related to endogenous primate, and infectious primate group) is located in an immune-complex pattern in some renal glomeruli of human SLE patients with lupus proliferative glomerulonephritis but is not detected in normal or pathological control human kidneys. This antigen cross-reacts with p30 interspecies determinants shared by the four chief virus groups and cross-reacts with a partially purified antigen extracted from human SLE spleen. The human SLE spleen antigen cross-reacts with p30 group antigen of RD-114 virus but not of feline or murine viruses. Some host immunoglobulins eluted from a human SLE kidney by acid-buffer show antibody-like activity against p30 group antigen of RD-114 virus but not of simian, feline, or murine viruses.

The influence of genetic and nongenetic factors on abnormalities of the immune response in systemic lupus erythematosus (SLE) was studied in 9 sets of twins in which one or both twins had SLE. Particular emphasis was placed on contrasting the results between the sibs of 3 monozygotic pairs discordant for clinical SLE. Depression of cell-mediated immunity, determined by lymphocyte blastogenic response to mitogens, was associated with the clinical expression of illness. In contrast, autoreactive antilymphocyte antibodies and lymphocyte tubuloreticular structures were found in both clinically affected and unaffected subjects and were more prominently associated with the presence of other serologic abnormalities. No evidence of antigens or cell surfaces determinants unique to affected sibs was encountered.