Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 3556-3558 |
| Number of pages | 3 |
| Journal | Infection and immunity |
| Volume | 61 |
| Issue number | 8 |
| State | Published - 1993 |
| Externally published | Yes |
ASJC Scopus subject areas
- Parasitology
- Microbiology
- Immunology
- Infectious Diseases