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The Journal of Immunology, 2002, 168: 1036-1041.
Copyright © 2002 by The American Association of Immunologists

Complement C4 Is Protective for Lupus Disease Independent of C31

Shirit Einav, Olga O. Pozdnyakova, Minghe Ma and Michael C. Carroll2

Center for Blood Research and Department of Pediatrics, Harvard Medical School, Boston, MA 02115

The role of complement C3 in mediating systemic lupus erythematosus (SLE) was examined using a double-knockout C3nullC4null Fas (CD95)-deficient mouse model. Results from this study reveal significant lymphadenopathy, splenomegaly, elevated titers of anti-nuclear Abs and anti-dsDNA Abs, an increased number of anti-dsDNA-producing cells in ELISPOT assay, as well as severe glomerulonephritis in the double-deficient mice. Based on these clinical, serological, and histological parameters, we find that autoimmune disease in the double-knockout group is similar in severity to that in C4null lpr mice, but not to that in C3null lpr mice. The development of severe SLE in the absence of both classical and alternative complement pathways suggests that it is the absence of C4, and not the presence of C3, that is critical in SLE pathogenesis. Thus, complement C4 provides an important protective role against the development of SLE.




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