[3] C3 circulates in an inactive form but can be activated in order to aid the immune system's response to a foreign invader.

[1] Patients with primary or secondary C3 deficiency generally displayed symptoms (i.e. suffered from infection) within the first 2 years of life.

[4] In some cases, primary and secondary C3 deficiency have been associated with the onset of rheumatic or renal (kidney) diseases, such as systemic lupus erythematosus[7] and membranoproliferative glomerulonephritis.

There have been recorded cases of C3 deficient patients that suffer only from immune complex-mediated diseases and not severe, recurrent infections.

[1] Treatment for C3 deficiency has generally involved the prescription of regular antibiotics intended to prevent infection.