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Blood, 1 August 2007, Vol. 110, No. 3, pp. 1064-1072. Prepublished online as a Blood First Edition Paper on April 20, 2007; DOI 10.1182/blood-2006-12-063982. This Article Full Text Full Text (PDF) Supplemental Figure All Versions of this Article: blood-2006-12-063982v1 110/3/1064    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 Burman, A. C. Articles by Hill, G. R. Search for Related Content PubMed PubMed Citation Articles by Burman, A. C. Articles by Hill, G. R. Related Collections Immunobiology Transplantation Cell Adhesion and Motility Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  TRANSPLANTATION IFN differentially controls the development of idiopathic pneumonia syndrome and GVHD of the gastrointestinal tract Angela C. Burman1, Tatjana Banovic1, Rachel D. Kuns1, Andrew D. Clouston2, Amanda C. Stanley1, Edward S. Morris1, Vanessa Rowe1, Helen Bofinger1, Renae Skoczylas1, Neil Raffelt1, Olivier Fahy3, Shaun R. McColl3, Christian R. Engwerda1, Kelli P. A. McDonald1, and Geoffrey R. Hill1,4 1 Queensland Institute of Medical Research, Herston; 2 Histopath Pathology, Strathfield, New South Wales; 3 Department of Microbiology and Immunology, University of Adelaide, Adelaide; 4 Department of Bone Marrow Transplantation, Royal Brisbane Hospital, Queensland, Australia Although proinflammatory cytokines are key mediators of tissue damage during graft-versus-host disease (GVHD), IFN has previously been attributed with both protective and pathogenic effects. We have resolved this paradox by using wild-type (wt), IFN–/–, and IFNR–/– mice as donors or recipients in well-described models of allogeneic stem cell transplantation (SCT). We show that donor-derived IFN augments acute GVHD via direct effects on (1) the donor T cell to promote T helper 1 (Th1) differentiation and (2) the gastrointestinal (GI) tract to augment inflammatory cytokine generation. However, these detrimental effects are overwhelmed by a protective role of IFN in preventing the development of idiopathic pneumonia syndrome (IPS). This is the result of direct effects on pulmonary parenchyma to prevent donor cell migration and expansion within the lung. Thus, IFN is the key cytokine differentially controlling the development of IPS and gastrointestinal GVHD after allogeneic SCT. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: The lung's friend, the gut's foe Gerhard Hildebrandt Blood 2007 110: 792-793. [Full Text] [PDF] This article has been cited by other articles: R. D. Kuns, E. S. Morris, K. P. A. MacDonald, K. A. Markey, H. M. Morris, N. C. Raffelt, T. Banovic, A. L. J. Don, V. Rowe, A. C. Burman, et al. Invariant natural killer T cell-natural killer cell interactions dictate transplantation outcome after {alpha}-galactosylceramide administration Blood, June 4, 2009; 113(23): 5999 - 6010. [Abstract] [Full Text] [PDF] K. A. Markey, T. Banovic, R. D. Kuns, S. D. Olver, A. L. J. Don, N. C. Raffelt, Y. A. Wilson, L. J. Raggatt, A. R. Pettit, J. S. Bromberg, et al. Conventional dendritic cells are the critical donor APC presenting alloantigen after experimental bone marrow transplantation Blood, May 28, 2009; 113(22): 5644 - 5649. [Abstract] [Full Text] [PDF] C. M. Capitini, S. Herby, M. Milliron, M. R. Anver, C. L. Mackall, and T. J. Fry Bone marrow deficient in IFN-{gamma} signaling selectively reverses GVHD-associated immunosuppression and enhances a tumor-specific GVT effect Blood, May 14, 2009; 113(20): 5002 - 5009. [Abstract] [Full Text] [PDF] H. Wang, W. Asavaroengchai, B. Yong Yeap, M.-G. Wang, S. Wang, M. Sykes, and Y.-G. Yang Paradoxical effects of IFN-{gamma} in graft-versus-host disease reflect promotion of lymphohematopoietic graft-versus-host reactions and inhibition of epithelial tissue injury Blood, April 9, 2009; 113(15): 3612 - 3619. [Abstract] [Full Text] [PDF] R. Das, X. Chen, R. Komorowski, M. J. Hessner, and W. R. Drobyski Interleukin-23 secretion by donor antigen-presenting cells is critical for organ-specific pathology in graft-versus-host disease Blood, March 5, 2009; 113(10): 2352 - 2362. [Abstract] [Full Text] [PDF] M. J. Carlson, M. L. West, J. M. Coghill, A. Panoskaltsis-Mortari, B. R. Blazar, and J. S. Serody In vitro-differentiated TH17 cells mediate lethal acute graft-versus-host disease with severe cutaneous and pulmonary pathologic manifestations Blood, February 5, 2009; 113(6): 1365 - 1374. [Abstract] [Full Text] [PDF] K. P A MacDonald, R. D Kuns, A. L. Don, S. D Olver, N. C Raffelt, K. A Markey, W. Alexander, A. W. Roberts, and G. R Hill SOCS3 Regulates Th1 Dependent Acute Graft-Versus Host Disease Blood (ASH Annual Meeting Abstracts), November 16, 2008; 112(11): 3513 - 3513. [Abstract] J.-S. Delisle, L. Gaboury, M.-P. Belanger, E. Tasse, H. Yagita, and C. Perreault Graft-versus-host disease causes failure of donor hematopoiesis and lymphopoiesis in interferon-{gamma} receptor-deficient hosts Blood, September 1, 2008; 112(5): 2111 - 2119. [Abstract] [Full Text] [PDF] T. Yi, D. Zhao, C.-L. Lin, C. Zhang, Y. Chen, I. Todorov, T. LeBon, F. Kandeel, S. Forman, and D. Zeng Absence of donor Th17 leads to augmented Th1 differentiation and exacerbated acute graft-versus-host disease Blood, September 1, 2008; 112(5): 2101 - 2110. [Abstract] [Full Text] [PDF]

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