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Clinical and Developmental Immunology
Volume 2012, Article ID 892687, 8 pages
Research Article

Inhibition of Arterial Allograft Intimal Hyperplasia Using Recipient Dendritic Cells Pretreated with B7 Antisense Peptide

1Department of General Surgery, Huashan Hospital, Fudan University, Shanghai 200040, China
2Department of General Surgery, Jiangsu Cancer Hospital and Cancer Research Institute, Nanjing 210009, China

Received 18 August 2011; Revised 9 October 2011; Accepted 28 October 2011

Academic Editor: Alexandre S. Basso

Copyright © 2012 Yu-Feng Yao et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Low expression or absence of dendritic cell (DC) surface B7 molecules can induce immune tolerance or hyporesponse. Whether DCs could induce indirect allogeneic-specific cross-tolerance or hyporesponse to recipient T cells remains unclear. Methods. Generated from C3H/He mice bone marrow cells pulsed with donor antigen from C57BL/6 mice, recipient DCs were incubated with B7 antisense peptide (B7AP). Immune regulatory activities were examined in vitro by a series of mixed lymphocyte reactions. Murine allogeneic carotid artery orthotopic transplantation was performed from C57BL/6 to C3H/He. Recipients were given B7AP-treated DCs 7 days before transplantation. Allograft pathological analysis was done 2 months after transplantation. Results. B7AP-pretreated DCs markedly inhibited T-cell proliferation compared with untreated group. Pretreated T cells exhibited markedly reduced response to alloantigen versus third-party antigen. Pathological analysis of arterial allografts demonstrated significant reduction of intimal hyperplasia in B7-AP pretreated group versus control. Conclusion. Blockade of B7 molecules by B7AP could induce indirect allogeneic-specific hyporesponse and inhibit arterial allograft intimal hyperplasia, which may be involved in future strategies for human allograft chronic rejection.