To evaluate the roles of CD4 and CD8 T lymphocytes in immunity to diss
eminated endothelial infection with Rickettsia conorii (Malish 7 strai
n), these T cell subsets were depleted or adoptively transferred into
subsequently infected C3H/HeN mice. CD4 T lymphocyte-depleted and sham
-depleted mice underwent a similar course of illness with a sublethal
rickettsial dose, cleared the infection by day 10, and recovered on da
ys 10 to 11. In contrast, mice depleted of CD8 lymphocytes or CD4 and
CD8 lymphocytes died or remained persistently infected through day 15
with the ordinarily sublethal dose. Endothelium was the major site of
rickettsial persistence, including sites in the vital organs, brain, a
nd lungs of CD8 lymphocyte-depleted mice. In nondepleted animals, CD8
T lymphocytes were observed in apposition to endothelial cells on day
10 at the time of rickettsial clearance. Adoptive transfer of immune C
D4 or CD8 T lymphocytes protected mice against a lethal dose of R. con
orii in the disseminated endothelial target model. Nonimmune CD4 or CD
8 lymphocytes and immune lymphocytes that had passed through columns t
hat depleted both CD4 and CD8 lymphocytes failed to protect mice again
st R. conorii. These studies represent the first analysis of the role
of T lymphocyte subsets in immunity to spotted fever group rickettsiae
and the first demonstration that clearance of spotted fever group ric
kettsiae from endothelial cells requires immune CD8 T lymphocytes.