@article {542826,
	title = {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.},
	journal = {Am J Pathol},
	volume = {157},
	number = {2},
	year = {2000},
	month = {2000 Aug},
	pages = {473-84},
	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-gamma 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.},
	keywords = {Animals, Antigen-Presenting Cells, Antigens, CD, Antigens, CD80, Antigens, CD86, B-Lymphocytes, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Chemokines, Cytokines, Female, Flow Cytometry, Gene Expression Regulation, Genotype, Graft Occlusion, Vascular, Graft Rejection, Heart Transplantation, Histocompatibility Antigens Class II, Immunohistochemistry, Macrophages, Male, Membrane Glycoproteins, Mice, Mice, Inbred C57BL, Time Factors, Transplantation, Homologous},
	issn = {0002-9440},
	doi = {10.1016/S0002-9440(10)64559-2},
	author = {Furukawa, Y and Mandelbrot, D A and Libby, P and Sharpe, A. H. and Mitchell, R N}
}
