The role of gamma-delta T cells in host resistance to Chlamydia tracho
matis was characterized by using a murine model of pneumonia caused by
the mouse pneumonitis agent (MoPn), murine C. trachomatis. At days 3
and 7 after infection, gamma-delta T-cell-deficient knockout mice had
significantly higher levels of MoPn in the lungs than did immunologica
lly intact controls. At day 20, paradoxically, gamma-delta T cell-defi
cient mice were more resistant to MoPn than were controls. This increa
sed resistance was not due to an increased production of toxic cytokin
es or interleukin-10 in controls on that day. Gamma-delta T cells play
a role in protection early in MoPn infection, but they may be deleter
ious later in infection, as has been observed in models of salmonella
and trypanosome infection.