Monocytosis and accelerated activation of lymphocytes in C1q‐deficient autoimmune‐prone mice

Summary C1q deficiency has been shown to accelerate spontaneous autoimmunity in mice. We studied the time course of activation of monocytes and lymphocytes in autoimmune and non‐autoimmune mice in the presence or absence of C1q as a disease accelerator. Autoimmune MRL\Mp.C1qa−\− and non‐autoimmune C57BL\6.C1qa−\− mice were analysed at various time points between 6 and 33 weeks of age and compared to strain‐ and age‐matched C1q‐sufficient controls. Splenic and peritoneal leucocytes were analysed by flow cytometry and plasma levels of immunoglobulin M (IgM), total IgG, IgG subclasses and IgM autoantibodies were measured. Both C1q‐deficient strains had significantly more splenic monocytes than their controls at all time points analysed. In addition, MRL\Mp.C1qa−\− but not C57BL/6.C1qa−\− mice developed splenic hypercellularity starting at about 12–17 weeks old, had signs of accelerated CD4+ T‐cell activation and showed a marked increase in splenic plasma cells and total serum IgM levels from about 22 weeks of age. The accelerated CD4+ T‐cell activation was not due to a direct inhibitory effect of C1q on T cells. These data show that C1q deficiency causes splenic monocytosis together with accelerated T‐cell activation in an autoimmune‐prone mouse strain.