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From the Departments of Medicine*
and
Pathology,
Brigham and Women’s Hospital,
Harvard Medical School, Boston, Massachusetts
Interleukin-10 (IL-10) is an anti-inflammatory helper T cell type 2
(Th2) cytokine that modulates Th1-type cytokine production. Graft
arterial disease (GAD) is a vascular obliterative process mediated via
the Th1 cytokine interferon-
(IFN-); allografts in
IFN--deficient animals do not develop GAD. We investigated the
effect of IL-10 and anti-IL-10 on GAD in murine heart transplants and
whether anti-IL-10 reestablishes GAD in IFN--deficient hosts. Major
histocompatibility complex class II-mismatched hearts were transplanted
for 8 weeks into wild-type or IFN--deficient mice. In one set of
experiments, wild-type hosts received daily administration of
phosphate-buffered saline (PBS) or increasing IL-10; in a subsequent
set of experiments, wild-type hosts received weekly
PBS, rat IgG, or anti-IL-10 monoclonal antibody;
IFN--deficient recipients received weekly PBS or anti-IL-10
monoclonal antibody. Explanted allografts were assessed for parenchymal
rejection and GAD, cytokine profiles, and
adhesion/costimulatory-molecule expression. Exogenous IL-10 resulted in
increased Th2-like cytokine production; nevertheless, it
exacerbated parenchymal rejection and GAD and increased
CD8+ infiltration. Anti-IL-10 did not significantly affect
the extent of rejection or GAD, cytokine profiles, or
immunohistology of the allografts in wild-type hosts. Adhesion molecule
(CD54 and CD106) expression was not diminished by IL-10
treatment, and costimulatory-molecule (CD80 and CD86)
expression was augmented by administration of exogenous IL-10.
Allografts in IFN--deficient recipients showed mild rejection and no
GAD, regardless of anti-IL-10 treatment. IL-10 in
vivo thus has markedly different effects than predicted from
in vitro experience. Although allografts develop
Th2-like cytokine profiles treatment with IL-10 causes exacerbated
rejection and GAD.
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