Primary murine Chlamydia trachomatis pneumonia in B-cell-deficient mice.

Mice were rendered deficient in B-cell activity by treatment with anti-mu antibody from birth. These animals were then infected intranasally with murine Chlamydia trachomatis (murine pneumonitis agent [MoPn]). They produced neither local nor systemic antibody to MoPn but had intact delayed-type hypersensitivity to MoPn. Anti-mu-treated mice were not significantly more susceptible to primary invasive infection with MoPn than were control mice, and unrestricted multiplication with MoPn did not occur. The dominant immune response controlling this type of infection is not likely to be antibody.