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Center for Immunology and Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110
Listeriosis in mice with the SCID mutation results in a chronic
infection. The chronic infection is characterized by abundant
granulomas and neutrophil infiltrates. Both lesions were particularly
noticeable in the liver. In the liver, about 95% are granulomas with
5% microabscesses involving intrahepatic infection. The majority of
Listeria resided in membrane-bound vacuolar structures of
the macrophages and not in the cytosol. Three manipulations resulted in
alterations in the equilibrium between granulomas and liver
microabscesses, with massive transfer of the infection to the
hepatocyte and dissolution of the granulomas: depletion of neutrophils
and neutralization of IFN-
and TNF-
. We did not find a role for
IL-12, IL-10, or nitric oxide. Adoptive transfer studies showed a
decisive role for both CD4+ and CD8+ T cells
for an effective immune response, i.e., clearance of bacteria,
granuloma formation with lymphocytes, and disappearance of
microabscess. Clearance of Listeria was induced by transfer
of CD8+ T cells from mice with targeted disruption of the
IFN- structural gene (IfgTM1KO), even in the presence of
neutralizing mAb to IFN-. In marked contrast, transfer of
CD4+ T cells from IfgTM1KO mice exacerbated the infection
in the chronically infected SCID mice, resulting in increased mortality
with dissolution of the granulomas and severe hepatic infection with
neutrophil infiltration. Thus, these data indicate that both
IFN--dependent and -independent mechanisms are operative in the
context of a chronic listerial infection.
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