The current studies were undertaken to characterize the cDNA for wild-type canine C3 and identify the molecular basis for hereditary canine C3 deficiency.
Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity.
Current knowledge of the molecular and cellular basis of complement C3 deficiency indicates that C3 deficiency is caused by numerous molecular genetic mutations that include splicing defects, a partial gene deletion, and a critical amino acid substitution.
The occurrence of an immune complex-like disease (with characteristics of the HCVS) in a patient with a familial deficiency of C3 suggests that the preexisting C3 deficiency may predispose such persons to certain diseases.