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Blood, 1 September 2004, Vol. 104, No. 5, pp. 1565-1573. Prepublished online as a Blood First Edition Paper on May 18, 2004; DOI 10.1182/blood-2004-01-0328. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-01-0328v1 104/5/1565    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Anderson, B. E. Articles by Shlomchik, M. J. Search for Related Content PubMed PubMed Citation Articles by Anderson, B. E. Articles by Shlomchik, M. J. Related Collections Immunobiology Transplantation Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  TRANSPLANTATION Recipient CD4+ T cells that survive irradiation regulate chronic graft-versus-host disease Britt E. Anderson, Jennifer M. McNiff, Catherine Matte, Ionna Athanasiadis, Warren D. Shlomchik, and Mark J. Shlomchik From the Section of Immunobiology, Department of Dermatology, Section of Medical Oncology, and Department of Laboratory Medicine, Yale University School of Medicine, New Haven, CT. Chronic graft-versus-host disease (cGVHD) is an increasingly common cause of morbidity and mortality in allogeneic stem cell transplantation (alloSCT). Relative to acute GVHD (aGVHD), much less is understood about cGVHD. Using the B10.D2 BALB/c murine cGVHD model, which shares critical pathologic features with human cGVHD, we find that radiation-resistant host T cells regulate cGVHD. We initially observed that recipients lacking all lymphocytes developed accelerated and more severe cGVHD. Using genetically deficient recipients, we determined that +CD4+ T cells were required to regulate cGVHD. Increased cGVHD severity was not due to the absence of T cells per se. Rather, the potency of regulation was proportional to host T-cell receptor (TCR) diversity. Only CD4+CD25+, and not CD4+CD25-, host T cells ameliorated cGVHD when added back, indicating that host T cells acted not via host-versus-graft activity or by reducing homeostatic proliferation but by an undefined regulatory mechanism. Thus, preparative regimens that spare host CD4+CD25+ T cells may reduce cGVHD. Donor CD4+CD25+ T cells also reduced cGVHD. Depletion of CD4+CD25+ cells from the inoculum exacerbated disease, whereas transplantation of additional CD4+CD25+ cells protected against severe cGVHD. Additional CD4+CD25+ cells also promoted healing of established lesions, suggesting that their effects persist during the evolution of cGVHD. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Zhao, C. Zhang, T. Yi, C.-L. Lin, I. Todorov, F. Kandeel, S. Forman, and D. Zeng In vivo-activated CD103+CD4+ regulatory T cells ameliorate ongoing chronic graft-versus-host disease Blood, September 1, 2008; 112(5): 2129 - 2138. [Abstract] [Full Text] [PDF] B. E. Anderson, P. A. Taylor, J. M. McNiff, D. Jain, A. J. Demetris, A. Panoskaltsis-Mortari, A. Ager, B. R. Blazar, W. D. Shlomchik, and M. J. Shlomchik Effects of donor T-cell trafficking and priming site on graft-versus-host disease induction by naive and memory phenotype CD4 T cells Blood, May 15, 2008; 111(10): 5242 - 5251. [Abstract] [Full Text] [PDF] C. Matte-Martone, J. Liu, D. Jain, J. McNiff, and W. D. 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