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T Cell-Deficient Mice Exhibit Reduced Disease Severity and Decreased Inflammatory Response in the Brain in Murine Neurocysticercosis
Department of Microbiology, University of Texas Health Science Center, San Antonio, TX 78229
In a recently developed mouse model for neurocysticercosis, the
immune response was characterized by a massive influx of 
T cells
and a type 1 pathway of cytokine expression. To understand the role of
T cells during this infection, the cellular and cytokine
response was analyzed in mice that lack T cells
(TCR-/-). In TCR-/- mice,
Mesocestoides corti metacestodes preferentially invaded
the extraparenchymal areas of the brain. Furthermore, parasites were
able to escape from the brain and establish a systemic infection with
liver and peritoneal involvement. Immunopathological studies indicated
that TCR-/- mice develop little inflammatory response
and less neurological symptomatology. Significantly reduced numbers of
T cells, macrophages, dendritic cells, and mast cells were present in
the brain. The cytokine response in the brain of
TCR-/- mice appears to be a mixed type1/type 2
response with low levels of IL-2, IL-4, IL-10, IL-12, IL-13, IL-15, and
IFN-. To further investigate the immunological significance of this
cell population, T cells were adoptively transferred into
intracranially infected TCR-/- mice. T cells
were specifically recruited into the CNS in response to this parasitic
infection, and they were able to target the infected brain within
12 h after transfer. These results suggest that T cells are
key players in the immune response elicited during this CNS infection
and direct a type 1 response in wild-type mice upon
infection.
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