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*
Department of Pathobiology, University of Pennsylvania, Philadelphia, PA, 19104; and
Bristol Myers Squibb Pharmacology Research Institute, Princeton, NJ 08543
Infection of C57BL/6 mice with Toxoplasma gondii
leads to chronic encephalitis characterized by infiltration into the
brain of T cells that produce IFN-
and mediate resistance to the
parasite. Our studies revealed that expression of B7.1 and B7.2 was
up-regulated in brains of mice with toxoplasmic encephalitis (TE).
Because CD28/B7-mediated costimulation is important for T cell
activation, we assessed the contribution of this interaction to the
production of IFN- by T cells from brains and spleens of mice with
TE. Stimulation of splenocytes with Toxoplasma Ag or
anti-CD3 mAb resulted in production of IFN-, which was inhibited
by 90% in the presence of CTLA4-Ig, an antagonist of B7 stimulation.
However, production of IFN- by T cells from the brains of these mice
was only slightly reduced (20%) by the addition of CTLA4-Ig. To
address the role of the CD28/B7 interaction during TE, we compared the
development of disease in C57BL/6 wild-type (wt) and
CD28-/- mice. Although the parasite burden was similar in
wt and CD28-/- mice, CD28-/- mice developed
less severe encephalitis and survived longer than wt mice. Ex vivo
recall responses revealed that mononuclear cells isolated from the
brains of chronically infected CD28-/- mice produced less
IFN- than wt cells, and this correlated with reduced numbers of
intracerebral CD4+ T cells in CD28-/- mice
compared with wt mice. Taken together, our data show that resistance to
T. gondii in the brain is independent of CD28 and
suggest a role for CD28 in development of immune-mediated pathology
during TE.
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