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Blood, 15 June 2005, Vol. 105, No. 12, pp. 4885-4891. Prepublished online as a Blood First Edition Paper on March 3, 2005; DOI 10.1182/blood-2004-12-4980. This Article Full Text (PDF) All Versions of this Article: 2004-12-4980v1 105/12/4885    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Tivol, E. Articles by Drobyski, W. R Search for Related Content PubMed PubMed Citation Articles by Tivol, E. Articles by Drobyski, W. R Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted January 3, 2005 Accepted February 10, 2005 Emergent autoimmunity in graft versus host disease Elizabeth Tivol, Richard Komorowski, and William R Drobyski* Bone Marrow Transplant Program and the Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA Department of Pathology, Medical College of Wisconsin, Milwuakee, WI, USA * Corresponding author; email: bill{at}bmt.mcw.edu. Donor T cell recognition of host alloantigens presented by host antigen presenting cells (APCs) is necessary for the induction of GVHD, but whether direct alloreactivity is sufficient for the propagation of GVHD is unknown. In this study, we demonstrate that GVHD cannot be effectively propagated through the direct pathway of allorecognition. Rather, donor T cell recognition of antigens through the indirect pathway is necessary for the perpetuation of GVHD. Furthermore, GVHD results in the breaking of self tolerance resulting in the emergence of donor T cells that can cause autoimmune disease in syngeneic recipients. Notably, GVHD-induced autoreactivity is donor APC-dependent, transferable into secondary hosts, and involves cells of the innate immune system. These results indicate that donor T cell-mediated pathological damage during GVHD becomes donor APC-dependent, and provide a mechanistic explanation for the longstanding observation that GVHD is associated with autoimmune clinical manifestations. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Chronic graft-versus-host disease: a breakdown of self-tolerance? Allan D. Hess Blood 2005 105: 4548-4549. [Full Text] [PDF] This article has been cited by other articles: D. Daoussis, S.-N. C. Liossis, A. C. 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[Abstract] [Full Text] [PDF] D. R. Sekiguchi, L. Yunk, D. Gary, D. Charan, B. Srivastava, D. Allman, M. G. Weigert, and E. T. L. Prak Development and Selection of Edited B Cells in B6.56R Mice. J. Immunol., June 1, 2006; 176(11): 6879 - 6887. [Abstract] [Full Text] [PDF] E. A. Copelan Hematopoietic stem-cell transplantation. N. Engl. J. Med., April 27, 2006; 354(17): 1813 - 1826. [Full Text] [PDF] C. Zhang, I. Todorov, Z. Zhang, Y. Liu, F. Kandeel, S. Forman, S. Strober, and D. Zeng Donor CD4+ T and B cells in transplants induce chronic graft-versus-host disease with autoimmune manifestations Blood, April 1, 2006; 107(7): 2993 - 3001. [Abstract] [Full Text] [PDF]

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