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Nephrology Dialysis Transplantation 2007 22(5):1293-1296; doi:10.1093/ndt/gfl830
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The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

Costimulation blockade—what will the future bring?

Flavio Vincenti

University of California, San Francisco, Kidney Transplant Service, San Francisco, California

Correspondence and offprint requests to: Flavio Vincenti, MD, Professor of Clinical Medicine and Surgery, University of California, San Francisco, Kidney Transplant Service, 505 Parnassus Avenue, Room 884M, San Francisco, CA 94143-0780. Email: vincentif@surgery.ucsf.edu

Keywords: belatacept; costimulation blockade; fusion receptor proteins

The first 150 words of the full text of this article appear below.



   Introduction
 
The long and torturous road in the clinical development of costimulation blockade came to fruition in 2005, with the approval of CTLA4Ig (abatacept) for rheumatoid arthritis and the publication of the promising results of the phase II trial in kidney transplantation of belatacept (previously referred to as LEA29Y) [1–3]. Harnessing the therapeutic potential of costimulation blockade, an essential signal for T-cell activation, has been the focus of translational research for the past 25 years [1]. However, the promising early results of either prolongation graft survival or induction of tolerance using costimulation blockade in transplantation experiments in rodents could not be reproduced in non-human primates (NHP) [4,5]. While the discrepancies between the outcome of transplantation in rodents and NHP treated with CTLA4Ig are complex and multifactorial (i.e. differences in immune systems, repertoire of memory T cells and environmental exposure), it also became apparent . . . [Full Text of this Article]



   Chronic protein therapy—a novel delivery of immunosuppression
 


   Costimulation blockade and T regulatory cells
 


   Conclusion
 


   Disclosure
 

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