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Blood, 15 July 2004, Vol. 104, No. 2, pp. 586-593. Prepublished online as a Blood First Edition Paper on April 6, 2004; DOI 10.1182/blood-2003-12-4259. This Article Full Text (PDF) All Versions of this Article: 2003-12-4259v1 104/2/586    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 Hildebrandt, G. C Articles by Cooke, K. R Search for Related Content PubMed PubMed Citation Articles by Hildebrandt, G. C Articles by Cooke, K. R Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 15, 2003 Accepted March 16, 2004 Donor-derived TNF regulates pulmonary chemokine expression and the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation Gerhard C Hildebrandt, Krystyna M Olkiewicz, Leigh A Corrion, Yayi Chang, Shawn G Clouthier, Chen Liu, and Kenneth R Cooke* Department of Pediatrics, University of Michigan, Ann Arbor, MI, USA Department of Pathology, University of Michigan, Ann Arbor, MI, USA Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA Department of Pathology, University of Florida School of Medicine, Gainesville, FL, USA * Corresponding author; email: krcooke{at}med.umich.edu. Idiopathic pneumonia syndrome (IPS) is a significant cause of mortality after allogeneic bone marrow transplantation (allo-BMT) and TNF is a significant effector molecule in this process. However, the relative contribution of donor- versus host-derived TNF to the development of IPS has not been elucidated. Using a lethally irradiated parentF1 mouse IPS model, we showed that 5 weeks after transplant allo-BMT recipients developed significant lung injury compared to syngeneic controls, which was associated with increased BAL fluid levels of TNF, elevated numbers of donor-derived TNF-secreting T cells and increased pulmonary macrophage production of TNF to LPS stimulation. Allo-BMT with TNF-/- donor cells resulted in significantly reduced IPS severity, whereas utilization of TNF deficient mice as BMT recipients had no effect on IPS. We next determined that TNF secretion from both donor accessory cells (monocytes/macrophages) and T cells significantly contributed to the development of IPS. Importantly, the absence of donor T cell-derived TNF resulted in a significant decrease in inflammatory chemokine production in the lung and near complete abrogation of IPS. Collectively, these data demonstrate that donor TNF is critical to the development of IPS and reveal a heretofore unknown mechanism for T cell-derived TNF in the evolution of this process. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: 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] G. A. Yanik, V. T. Ho, J. E. Levine, E. S. White, T. Braun, J. H. Antin, J. Whitfield, J. Custer, D. Jones, J. L. M. Ferrara, et al. The impact of soluble tumor necrosis factor receptor etanercept on the treatment of idiopathic pneumonia syndrome after allogeneic hematopoietic stem cell transplantation Blood, October 15, 2008; 112(8): 3073 - 3081. [Abstract] [Full Text] [PDF] N. Mauermann, J. Burian, C. von Garnier, S. Dirnhofer, D. Germano, C. Schuett, M. Tamm, R. Bingisser, U. Eriksson, and L. Hunziker Interferon-{gamma} Regulates Idiopathic Pneumonia Syndrome, a Th17+CD4+ T-Cell-mediated Graft-versus-Host Disease Am. J. Respir. Crit. Care Med., August 15, 2008; 178(4): 379 - 388. [Abstract] [Full Text] [PDF] H. M. Marriott, P. G. Hellewell, S. S. Cross, P. G. Ince, M. K. B. Whyte, and D. H. Dockrell Decreased Alveolar Macrophage Apoptosis Is Associated with Increased Pulmonary Inflammation in a Murine Model of Pneumococcal Pneumonia J. Immunol., November 1, 2006; 177(9): 6480 - 6488. [Abstract] [Full Text] [PDF] C. A. Wysocki, A. Panoskaltsis-Mortari, B. R. Blazar, and J. S. Serody Leukocyte migration and graft-versus-host disease Blood, June 1, 2005; 105(11): 4191 - 4199. [Abstract] [Full Text] [PDF] M. Shukla, S. Yang, C. Milla, A. Panoskaltsis-Mortari, B. R. Blazar, and I. Y. Haddad Absence of host tumor necrosis factor receptor 1 attenuates manifestations of idiopathic pneumonia syndrome Am J Physiol Lung Cell Mol Physiol, May 1, 2005; 288(5): L942 - L949. [Abstract] [Full Text] [PDF] G. C. Hildebrandt, K. M. Olkiewicz, S. Choi, L. A. Corrion, S. G. Clouthier, C. Liu, J. S. Serody, and K. R. Cooke Donor T-cell production of RANTES significantly contributes to the development of idiopathic pneumonia syndrome after allogeneic stem cell transplantation Blood, March 15, 2005; 105(6): 2249 - 2257. [Abstract] [Full Text] [PDF]

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