The preceding paper describes the inhibition by chloramphenicol of "priming" for the secondary antibody response by a standard dose of antigen (1). For full effect, the inhibiting drug must have been administered from the day of stimulus continuously for 10 to 14 days thereafter. This paper examines this phenomenon in more detail; the results confirm the earlier experiments and indicate that priming can be effected within 3 hours after a subcutaneous injection of antigen.Little work has been done until recently on the effect of chloramphenicol on antibody formation. Slanetz (2) reported a decrease in the agglutinin response in rats to Salmonella enteritidis when they were fed chloramphenicol 1 for long periods. But neither Watson (3), nor Zhuravleva and Gorchakova (4) could demonstrate such an effect in rabbits given bacterial antigens and chloramphenicol in doses of 20 to 55 mg/kg/day. And Nathan eb al. (5) also failed to demonstrate impairment of the agglutinin response to sheep erythrocytes in mice given 250 mg/kg/day. These contraAictory findings were resolved, in part, when Ambrose and Coons (6) recently reported that chloramphenicol in bactericidal concentrations completely inhibited the secondary antibody response in tissue culture. They found that its inhibitory action was effective only during the first stages of the response, before the synthesis of antibody was well under way, and that it was without effect later, during the period when most of the antibody was produced. This led them to suggest that chloramphenicol interferes with messenger RNA, and that the apparent insensitivity of mammalian systems was due to the greater stability of mammalian messenger. In line with this suggestion was the report by Weisberger et al. (7), working also with a mammalian system, reticulocyte ribosomes. They found that chloramphenicol in a concen-