Deficiency of C1q, the initiator of the complement classical pathway, is associated with the development of systemic lupus erythematosus (SLE). Explaining this association in terms of abnormalities in the classical pathway alone remains problematic because C3 deficiency does not predispose to SLE. Here, using a mouse model of SLE, we demonstrate that C1q, but not C3, restrains the response to self-antigens by modulating the mitochondrial metabolism of CD8(+) T cells, which can themselves propagate autoimmunity. C1q deficiency also triggers an exuberant effector CD8(+) T cell response to chronic viral infection leading to lethal immunopathology. These data establish a link between C1q and CD8(+) T cell metabolism and may explain how C1q protects against lupus, with implications for the role of viral infections in the perpetuation of autoimmunity.