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, TNF-
, and Inducible Nitric Oxide Synthase1
Department of Immunology and Infectious Diseases, Research Institute, Palo Alto Medical Foundation, Palo Alto, CA 94301; and Division of Infectious Diseases and Geographic Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305
The role of B cells in resistance against Toxoplasma
gondii was studied using B cell-deficient (µMT) mice.
Following peroral infection with 10 cysts of the ME49 strain, all µMT
mice survived the acute stage of the infection but died between 3 and 4
wk after infection. In contrast, all control mice were alive at 8 wk
after infection. At the stage during which µMT animals succumbed to
the infection, parasite replication and pathology were most evident in
their brains; small numbers of tachyzoites were also detectable in
their lungs. Significantly greater numbers of T. gondii
cysts and areas of inflammation associated with tachyzoites were
observed in brains of µMT than in control mice. Large areas of
necrosis associated with numerous tachyzoites were observed only in
brains of µMT mice. Anti-T. gondii IgG Abs were
detected only in sera of control mice, whereas similar levels of
IFN-
were detected in sera of both strains of mice. Amounts of mRNA
for IFN-, IL-10, and inducible NO synthase in the brain did not
differ between infected µMT and control mice. Expression of mRNA for
TNF-
was increased in brains of µMT mice. Administration of
polyclonal rabbit anti-T. gondii IgG Ab prevented
early mortality and pathology associated with tachyzoites in the brain
in the infected µMT mice. These results indicate that B cells play an
important role, most likely through their production of specific Abs,
in resistance to persistent active (tachyzoite) infection with
T. gondii in mice, especially in the brain and
lung.
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