Association of B7-1 co-stimulation with the development of graft arterial disease: Studies using mice lacking B7-1, B7-2 or B7-1/B7-2

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Abstract

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-γ 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. © 2000 American Society for Investigative Pathology.

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APA

Furukawa, Y., Mandelbrot, D. A., Libby, P., Sharpe, A. H., & Mitchell, R. N. (2000). Association of B7-1 co-stimulation with the development of graft arterial disease: Studies using mice lacking B7-1, B7-2 or B7-1/B7-2. American Journal of Pathology, 157(2), 473–484. https://doi.org/10.1016/S0002-9440(10)64559-2

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