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Departments of
*
Medicine and
Pathology, Channing Laboratory, Brigham and Women’s Hospital, Boston, MA 02115;
Division of Infectious Disease, Dana-Farber Cancer Institute, Boston, MA 02115;
§
Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115; and
¶
Maxwell Finland Laboratory, Boston University School of Medicine, Boston, MA 02118
Little is known regarding the mechanism by which T cells control
intraabdominal abscess formation. Treating animals with polysaccharide
A (PS A) from Bacteroides fragilis shortly before or
after challenge protects against abscess formation subsequent to
challenge with different abscess-inducing bacteria. Although bacterial
polysaccharides are considered to be T cell-independent Ags, T cells
from PS A-treated animals mediate this protective activity. In the
present study, we demonstrate that CD4+ T cells transfer PS
A-mediated protection against abscess formation, and that a soluble
mediator produced by these cells confers this activity. Cytokine mRNA
analysis showed that T cells from PS A-treated animals produced
transcript for IL-2, IFN-
, and IL-10, but not for IL-4. The addition
of IL-2-specific Ab to T cell lysates taken from PS A-treated animals
abrogated the ability to transfer protection, whereas the addition of
Abs specific for IFN- and IL-10 did not affect protection. Finally,
administration of rIL-2 to animals at the time of bacterial challenge
prevented abscess formation in a dose-dependent manner. These data
demonstrate that PS A-mediated protection against abscess formation is
dependent upon a CD4+ T cell-dependent response, and that
IL-2 is essential to this immune mechanism.
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