SLE is characterized by overproduction of various types of antibodies. Under certain circumstances, antibodies aiming some of the neoepitopes of the complement system can be seen. Neoepitopes are not present in the native proteins, but they appear after the structural change of the complement system. One of these antibodies binds the activated product C3 called iC3b; however, its possible part in the pathogenesis of a disease is unknown. Some of the antibodies to the component of the complement system are more significant. One of them is the C3 nephritic factor connected with partial lipodystrophy and with a certain form of mesangial glomerulonephritis. This factor also rarely appears in patients with SLE. Another antibody targets the C1 inhibitor and appears in some patients with lymphomas. Anti-C1q antibodies are present in approximately one third of the patients with lupus, who often have high clinical activity of the disease, and particularly, renal involvement. In the presence of high titers of anti C1q antibodies also the levels of C1q and C4 components of the complement system are also usually low. The levels of the C3 component of the complement system are only slightly lowered or sometimes not at all in SLE as already discussed above. However, according to the findings in our study, patients with higher anti-C1q antibodies seem to show the tendency to have lower serum levels of C3. The presence of the anti-C1q antibodies is not limited or specific just for SLE or lupus nephritis. For the first time, they were described in HUVS (Hypocomplementemic Urticar Vasculitis Syndrome), later in Felty´s syndrome, rheumatoid vasculitis, in hepatitis C or in aging population. The association between the presence of anti-C1q antibodies and the consumption of protein in the classic way of complement activation seen in SLE and in HUVS raises the question, whether these antibodies cause or amplify the classic way of complement activation. The alternative theory sees the anti-C1q antibodies as a mere product of this activation itself, which creates the neoepitopes in the molecule C1q.