Host defense against murine Chlamydia trachomatis (mouse pneumonitis agent [MoPn]) in a murine model was investigated. Gamma interferon (IFN-γ) was produced in the lungs by both MoPn-susceptible nude athymic (nu/nu) and MoPn- resistant heterozygous (nu/+) mice. In vivo depletion of IFN-γ in nu/nu mice led to exacerbation of infection. Fluorescence-activated cell sorter analysis disclosed induction of GL3 antibody-positive cells (putatively γ/δ+ T cells) in nu/nu mouse lung during infection with MoPn. Treatment of nu/nu mice in vivo with antibody to NK cells (anti-asialo GM1 antibody) or to γ/δ cells (UC7-13D5) did not significantly decrease IFN-γ production in the lung. However, treatment of severe combined immunodeficiency mice (which lack γ/δ cells) with antibody to NK cells significantly reduced lung IFN-γ levels.
ASJC Scopus subject areas
- Infectious Diseases