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The C3b inactivator (C3bINA) contained in whole human serum has been purified by sequential diethylaminoethyl- and carboxymethyl-cellulose chromatography and polyacrylamide disc gel electrophoresis to yield a material which produces antibody to C3bINA when used to immunize rabbits. The specificity of the antibody for C3bINA was established by its ability to neutralize C3bINA activity in free solution. On Ouchterlony analysis against normal plasma, this anti-C3bINA gives a line of complete identity with antibody to conglutinogen activating factor (KAF) and a reaction of complete non-identity with antibody to β-2-glycoprotein II, the protein which has been found by others to be the C3 proactivator of the alternate pathway for activation of the late complement components.

Publisher Summary Nonspecific effector systems of inflammation appear to be phylogenetically more ancient than adaptive immunity. Late complement components, for example, have been recognized in invertebrates lacking any known immunoglobulins. With the evolution of adaptive immunity in the vertebrates, preexisting effector systems of inflammation appear to have been adapted to immunological activation, and specific immune responses, relatively feeble in themselves, are markedly amplified. The kinin-forming system and the complement sequence also have a capacity for self-amplification. Further, the systems involved in the inflammatory response are marked by a striking degree of mutual enhancement. Complex interrelationships are also apparent in the cellular aspects of inflammation and in the synergism between humoral and cellular contributions. The inherent tendency of these plasma systems of inflammation to amplify makes control factors critical in limiting the extent of inflammation and in preventing spontaneous activation. This chapter focuses on the reactions and interactions of two of the plasma effector systems: (1) complement and (2) the kinin-forming sequence.

The review of antimalarial pharmacology and the examination of results in recent studies of malaria in Vietnam revealed that (1) quinoline derivatives have multiple actions which include interference with nucleic acid replication and glucose metabolism; (2) sulfonamides and sulfones competitively antagonize aminobenzoic acid (PABA); and (3) folic acid reductase inhibitors interfere with the conversion of folic acid to folinic acid. No single agent produced satisfactory cure rates in recent trials with malaria in Vietnam. A combination of quinine and pyrimethamine appeared to give additive results. A combination of pyrimethamine and a sulfonamide gave superior results consistent with their proved synergism. A combination therapy of a long-acting sulfonamide with pyrimethamine, possibly with the addition of quinine, is recommended as the most rational therapy at this time.