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*
Department of Immunology and Infectious Diseases, Research Institute, Palo Alto Medical Foundation, Palo Alto, CA 94301;
Department of Medicine, Division of Infectious Diseases and Geographic Medicine, Stanford University School of Medicine, Stanford, CA 94305;
Laboratory of Parasitic Diseases, Immunobiology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; and
§
Department of Immunobiology, DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304
The role for IL-10 in the immunopathogenesis of acute toxoplasmosis
following peroral infection was examined in both genetically
susceptible C57BL/6 and resistant BALB/c mice. C57BL/6-background
IL-10-targeted mutant (IL-10-/-) mice all died in 2 wk
after infection with 20 cysts of the ME49 strain, whereas only 20% of
control mice succumbed. Histological studies revealed necrosis in the
small and large intestines and livers of infected
IL-10-/- mice. The necrosis in the small intestine was
the most severe pathologic response and was not observed in control
mice. Treatment of infected IL-10-/- mice with either
anti-CD4 or anti-IFN-
mAb prevented intestinal pathology and
significantly prolonged time to death. Treatment of these animals with
anti-IL-12 mAb also prevented the pathology. Significantly greater
amounts of IFN- mRNA were detected in the lamina propria lymphocytes
obtained from the small intestine of infected IL-10-/-
mice than those from infected control mice. In common with
C57BL/6-background IL-10-/- mice, BALB/c-background
IL-10-/- mice all died developing intestinal pathology
after infection. Control BALB/c mice all survived even after infection
with 100 cysts and did not develop the intestinal lesions. Treatment
with anti-IFN- mAb prevented the pathology and prolonged time to
death of the infected IL-10-/- mice. These results
strongly suggest that IL-10 plays a critical role in down-regulating
IFN- production in the small intestine following sublethal peroral
infection with Toxoplasma gondii and that this
down-regulatory effect of IL-10 is required for prevention of
development of IFN--mediated intestinal pathology and mortality in
both genetically resistant BALB/c and susceptible C57BL/6
mice.
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