ALS and several ‘normal proteins’ were seen to be equally effective in suppressing anaphylactic response to primary challenge with heterologous antigen but response to secondary challenge remained unaltered. Challenge of ALS-treated mice with homologous ALS indicated that only a mild sensitivity had been engendered but animals nonspecifically suppressed and challenged with the homologous suppressant were acutely sensitive. The former probably is due to specific suppression of the antibody-producing lymphocytes; a single small dose of ALS given with an adjuvant was effective in sensitizing mice. Multiple precipitins against the suppressant were identified by immunodiffusion in the sera of mice of those groups suppressed by ALS or ‘normal protein’. Precipitin lines failed to appear after a single injection of a low dose of antigen in pertussis vaccine or Freund’s complete adjuvant even though the anaphylactic death rate of these mice was invariably high. Passive cutaneous anaphylaxis followed development of active anaphylaxis. Sera obtained just prior to primary challenge (10 days postsensitization) no longer gave a singificant PCA reaction following treatment with 2-ME. These findings presuppose the presence of a skin-sensitizing form of IgM, a low-titered reaginic antibody or a sub-class of IgG. 2-ME had no effect on sera drawn just prior to secondary challenge (17 days postsensitization and 7 days postprimary c
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