Biosynthetic Defect in Monocytes from Human Beings with Genetic Deficiency of the Second Component of Complement

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Abstract
INVESTIGATIONS of the biosynthesis of complement proteins in vitro have provided preliminary information on the molecular basis of genetically determined complement deficiencies in man and laboratory animals.1 2 3 For example, evidence has been obtained that a specific defect in protein synthesis accounts for reduced serum concentrations of the natural inhibitor of the first component of complement in hereditary angioneurotic edema1 and of the fifth component (C5) and the fourth component (C4) in deficient mice2 and guinea pigs respectively.3 A hereditary deficiency of the second component of complement (C2), transmitted as an autosomal recessive, has been described in man.4 5 6 Most C2-deficient patients . . .