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Complement depletion of rats by cobra venom factor had only minor and variable effects on the hyperacute form of EAE. It appears likely that the exudation of polymorphonuclear leukocytes and massive amounts of fibrin in this condition is not dependent on complement. However, it is not possible to eliminate all traces of complement with cobra factor. Therefore, it is theoretically possible that small amounts of complement, too little to be detected by hemolytic activity or gel diffusion, might accumulate in the EAE lesions during the 1- to 3-day period in which they evolved. However, inhibition of the neutrophil accumulation of nephrotoxic serum glomerulitis attested to the efficacy of the cobra factor. This internal control provided evidence against the binding of C3 and terminal components, at least for the last 3 hr of development of EAE lesions. As C3 levels fall within 4 hr of the initial injection, it is most probable that complement depletion spanned the time during which EAE lesions developed.
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Levine et al. (1971) studied this question.
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