A single intratracheal instillation of liposomes containing dichloro methylene diphosphonate into rats eliminated greater than 80% of the alveolar macrophage (AM phi) population, and the population was not significantly renewed during the ensuing week. AM phi depletion markedly increased local antibody production in the lung wall in pre-primed animals exposed to antigen aerosols. However, AM phi depletion did not affect the normal development of protective tolerance (particularly in the IgE antibody class) to inhaled antigen in immunologically naive rats. These results are discussed in relation to regional control of immune responses in the upper vs. the lower respiratory tract.