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Prepublished online as a Blood First Edition Paper on January 2, 2003; DOI 10.1182/blood-2002-08-2465. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-08-2465v1 101/9/3714    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 Panoskaltsis-Mortari, A. Articles by Blazar, B. R. Search for Related Content PubMed PubMed Citation Articles by Panoskaltsis-Mortari, A. Articles by Blazar, B. R. Related Collections Immunobiology Phagocytes Transplantation Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 May 2003, Vol. 101, No. 9, pp. 3714-3721 TRANSPLANTATION Acceleration of idiopathic pneumonia syndrome (IPS) in the absence of donor MIP-1 (CCL3) after allogeneic BMT in mice Angela Panoskaltsis-Mortari, John R. Hermanson, Elizabeth Taras, O. Douglas Wangensteen, Jonathan S. Serody, and Bruce R. Blazar From the Department of Pediatrics, Division of Hematology-Oncology, Blood and Marrow Transplant Program, University of Minnesota, Minneapolis; the Department of Physiology, University of Minnesota, Minneapolis; and the Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill. Idiopathic pneumonia syndrome (IPS) is a significant cause of morbidity and mortality after bone marrow transplantation (BMT) in humans. We developed a murine IPS model in which lethal pre-BMT conditioning and allogeneic T cells results in the recruitment of host monocytes and then donor T cells into the lung by day 7 after BMT, concomitant with development of severe lung dysfunction. We reported the T cell-dependent production of the T cell-attracting chemokine macrophage inflammatory protein-1 (MIP-1) in the lungs of such recipient mice. We reasoned that MIP-1 might be a critical mediator of IPS. Lethally conditioned mice received transplants of major histocompatibility complex-disparate marrow and either wild-type (MIP-1+/+) or knockout (MIP-1/) spleen cells. Recipients of MIP-1/ cells exhibited accelerated mortality and a decrease in specific compliance that appeared earlier than in recipients of MIP-1+/+ cells. Donor CD4+ and CD8+ T cell expansion was increased in the spleens of recipients of MIP-1/ cells. Lungs of recipients of MIP-1/ cells had earlier recruitment of both T-cell subsets by day 3 after BMT, concomitant with the influx of cells expressing the cytolysins granzymes A and B. Monocyte recruitment was not altered. Levels of inflammatory cytokines were not increased and levels of T cell-attracting chemokines were decreased. The level of the anti-inflammatory cytokine interleukin 13 (IL-13) was lower in the serum and lungs of recipients of MIP-1/ cells, indicating a skewing toward a more inflammatory T helper cell type 1 (Th1) cytokine milieu. Donor-derived MIP-1 may play a role in allogeneic-induced IPS by limiting aggressive expansion of CD4+ and CD8+ T cells. © 2003 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. A. Wysocki, Q. Jiang, A. Panoskaltsis-Mortari, P. A. Taylor, K. P. McKinnon, L. Su, B. R. Blazar, and J. S. Serody Critical role for CCR5 in the function of donor CD4+CD25+ regulatory T cells during acute graft-versus-host disease Blood, November 1, 2005; 106(9): 3300 - 3307. [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] 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] C. A. Wysocki, S. B. Burkett, A. Panoskaltsis-Mortari, S. L. Kirby, A. D. Luster, K. McKinnon, B. R. Blazar, and J. S. Serody Differential Roles for CCR5 Expression on Donor T Cells during Graft-versus-Host Disease Based on Pretransplant Conditioning J. Immunol., July 15, 2004; 173(2): 845 - 854. [Abstract] [Full Text] [PDF] A. Panoskaltsis-Mortari, A. Price, J. R. Hermanson, E. Taras, C. Lees, J. S. Serody, and B. R. Blazar In vivo imaging of graft-versus-host-disease in mice Blood, May 1, 2004; 103(9): 3590 - 3598. [Abstract] [Full Text] [PDF] G. C. Hildebrandt, U. A. Duffner, K. M. Olkiewicz, L. A. Corrion, N. E. Willmarth, D. L. Williams, S. G. Clouthier, C. M. Hogaboam, P. R. Reddy, B. B. Moore, et al. A critical role for CCR2/MCP-1 interactions in the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation Blood, March 15, 2004; 103(6): 2417 - 2426. [Abstract] [Full Text] [PDF]

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