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-Induced Chemokine Mig1
,
Departments of
*
Urology and
Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195;
Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106; and
§
Department of Urology, Tokyo Women’s Medical School, Tokyo, Japan
Direct evidence that cytokines with chemoattractant properties for
leukocytes, chemokines, recruit alloantigen-primed T cells into
transplanted allografts has been lacking. We present evidence that
neutralization of a single chemokine inhibits T cell infiltration into
class II MHC-disparate murine allografts and acute rejection. The
chemokines IFN-
-inducible protein-10 and monokine induced by IFN-
(Mig) are expressed in allogeneic skin grafts during the late stages of
acute rejection. Survival of class II MHC-disparate
B6.H-2bm12 allografts is prolonged from day 14 to day 55
posttransplant when C57BL/6 recipients are given a short course
treatment with an antiserum to Mig. This treatment also inhibits T cell
and macrophage infiltration into the allografts. B6.H-2bm12
allografts are also not rejected by IFN--/- C57BL/6
recipients. Injection of Mig directly into B6.H-2bm12
grafts on IFN--deficient recipients restores T cell infiltration and
rejection. Therefore, the inability of IFN--deficient recipients to
reject the class II MHC-disparate allografts is due to the lack of
intraallograft Mig production and alloantigen-primed T cell recruitment
to the graft. These results indicate for the first time the potential
utility of chemokine neutralization strategies in preventing T cell
infiltration into allografts and abrogating acute
rejection.
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