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
| Autor: | Y, Furukawa, D A, Mandelbrot, P, Libby, A H, Sharpe, R N, Mitchell |
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| Rok vydání: | 2000 |
| Předmět: |
CD4-Positive T-Lymphocytes
Graft Rejection Male Time Factors Genotype Antigen-Presenting Cells CD8-Positive T-Lymphocytes Mice Antigens CD Animals Transplantation Homologous B-Lymphocytes Membrane Glycoproteins Macrophages Graft Occlusion Vascular Histocompatibility Antigens Class II Flow Cytometry Immunohistochemistry Mice Inbred C57BL Gene Expression Regulation B7-1 Antigen Cytokines Heart Transplantation Female B7-2 Antigen Chemokines Regular Articles |
| Zdroj: | The American journal of pathology. 157(2) |
| ISSN: | 0002-9440 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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