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-Inducible Protein-10-Dependent Mechanism1
Departments of
*
Surgery and
Medicine and Microbiology/Immunology, Northwestern University Medical School, Chicago, IL 60611;
DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304; and
Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114
The poor success in controlling small bowel (SB) allograft
rejection is partially attributed to the unique immune environment in
the donor intestine. We hypothesized that Ag-induced activation of
donor-derived T cells contributes to the initiation of SB allograft
rejection. To address the role of donor T cell activation in SB
transplantation, SB grafts from DO11.10 TCR transgenic mice (BALB/c,
H-2Ld+) were transplanted into BALB/c (isografts), or
single class I MHC-mismatched (Ld-deficient) BALB/c
H-2dm2 (dm2, H-2Ld-) mutant mice (allografts).
Graft survival was followed after injection of control or antigenic
OVA323–339 peptide. Eighty percent of SB allografts
developed severe rejection in mice treated with antigenic peptide,
whereas <20% of allografts were rejected in mice treated with control
peptide (p < 0.05). Isografts survived >30 days
regardless of OVA323–339 administration. Activation of
donor T cells increased intragraft expression of proinflammatory
cytokine (IFN-
) and CXC chemokine IFN--inducible protein-10 mRNA
and enhanced activation and accumulation of host NK and T cells in SB
allografts. Treatment of mice with neutralizing
anti-IFN--inducible protein-10 mAb increased SB allograft
survival in Ag-treated mice (67%; p < 0.05) and
reduced accumulation of host T cells and NK cells in the lamina propria
but not mesenteric lymph nodes. These results suggest that activation
of donor T cells after SB allotransplantation induces production of a
Th1-like profile of cytokines and CXC chemokines that enhance
infiltration of host T cells and NK cells in SB allografts. Blocking
this pathway may be of therapeutic value in controlling SB allograft
rejection.
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