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From the Department of Medicine,*
Cardiovascular
Division, Vascular Medicine and Atherosclerosis Unit and the Department
of Pathology,
Immunology Research Division,
Brigham and Women’s Hospital, Harvard Medical School,
Boston, Massachusetts
To investigate the roles of B7-1 and/or B7-2 co-stimulatory
molecule in the development of graft arterial disease (GAD),
major histocompatibility complex (MHC) class II-mismatched allograft
hearts were transplanted into wild-type,
B7-1-/-, B7-2-/-, or
B7-1/B7-2-/- recipient mice. Grafts were explanted at 4
or 8 weeks and used for histological and immunohistochemical
analyses, RNase protection assay, and flow cytometry of
graft infiltrating cells. Grafts in wild-type recipients showed
macrophage, recipient MHC class II, and B7 molecule
co-localization by immunohistochemistry to GAD lesions. Flow cytometry
revealed that CD11b(+) and MHC class II(+) graft infiltrating cells
expressed B7-1 more than B7-2, whereas B7-2 expression was
predominant in CD11b(-) cells at 4 and 8 weeks. GAD was significantly
attenuated in the allografts in B7-1-/- and
B7-1/B7-2-/- but not in B7-2-/- recipients
compared to wild-type hosts. Interferon-
mRNA levels were comparable
in all graft combinations, whereas interleukin-4 mRNA levels
decreased in grafts in B7-2 deficient hosts, but did not
correlate with GAD attenuation. The findings indicate distinct roles
for B7-1 and B7-2 co-stimulatory molecules in the development of
GAD, potentially because of differential expression of B7-1 and
B7-2 molecules on distinct stimulator and/or effector cell
populations.
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