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T Cells in the Brain and Alters Resistant Mice to Susceptible-Like Phenotype
From the Immunologie et Génétique des Maladies
Parasitaires,*
INSERM U399, Faculté de Médecine,
Université de la Mediterranee, La Timone, Marseille, France; and
the Departments of Medicine and
Microbiology
and
Pathology,
Dartmouth Medical School, Lebanon,
New Hampshire
In this study, we report that infection with
Plasmodium yoelii 17XL, a lethal strain of
rodent malaria, does not result in death in the DBA/2 strain of
mice. In contrast to BALB/c mice, DBA/2 mice developed
significantly less parasitemia and never manifested symptoms of
cerebral malaria (CM) on infection with this parasite.
Moreover, the histological changes evident in the brain of
susceptible BALB/c were absent in DBA/2 mice. Interestingly,
the resistant DBA/2 mice when treated with recombinant interleukin
(IL)-2, were found to develop CM symptoms and the infection
became fatal by 6 to 8 days after infection. This condition was
associated with an augmented interferon-
and nitric oxide
production. Unexpectedly, IL-10 levels were also elevated in
IL-2-treated DBA/2 mice during late stage of infection (at day 6 of
infection) whereas the inverse relationship between IL-10 and
interferon- or nitric oxide was maintained in the early stage of
infection (at day 3 after infection). The level of tumor necrosis
factor-
production was moderately increased in the late phase of
infection in these mice. Histology of brain from IL-2-treated mice
demonstrated the presence of parasitized erythrocytes and infiltration
of lymphocytes in cerebral vessels, and also displayed some
signs of endothelial degeneration. Confocal microscopical studies
demonstrated preferential accumulation of 
T cells in the
cerebral vessels of IL-2-treated and -infected mice but not in mice
treated with IL-2 alone. The cells recruited in the brain were
activated because they demonstrated expression of CD25 (IL-2R) and CD54
(intercellular adhesion molecule 1) molecules. Administration of
anti- mAb prevented development of CM in IL-2-treated mice until
day 18 after infection whereas mice treated with control antibody
showed CM symptoms by day 6 after infection. The information concerning
creating pathological sequelae and death in an otherwise resistant
mouse strain provides an interesting focus for the burden of
pathological attributes on death in an infectious
disease.
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