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 Blood, 15 January 2005, Vol. 105, No. 2, pp. 894-901.
Prepublished online as a Blood First Edition Paper on September 16, 2004; DOI 10.1182/blood-2004-05-1687.

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TRANSPLANTATION

Donor-derived IL-15 is critical for acute allogeneic graft-versus-host disease

Bradley W. Blaser, Sameek Roychowdhury, Daniel J. Kim, Noah R. Schwind, Darshna Bhatt, Weifeng Yuan, Donna F. Kusewitt, Amy K. Ferketich, Michael A. Caligiuri, and Martin Guimond

From The Integrated Biomedical Sciences Graduate Program, Division of Human Cancer Genetics, Department of Molecular Virology, Immunology and Medical Genetics, Department of Veterinary Biosciences, Division of Hematology and Oncology, Department of Internal Medicine, Division of Epidemiology and Biometrics, and the Comprehensive Cancer Center, The Ohio State University, Columbus, OH.

Interleukin-15 (IL-15) is a pleiotropic proinflammatory cytokine with inefficient posttranscriptional processing. We hypothesized that endogenous IL-15 could affect disease progression in the well-described C57Bl/6 (B6) -> (C57Bl/6 x DBA/2) F1 hybrid (B6D2F1) murine model of acute allogeneic graft-versus-host disease (GVHD). B6D2F1 allogeneic recipients received transplants of IL-15-/- B6 bone marrow cells or B6 bone marrow cells expressing a murine IL-15 transgene (IL-15 tg) modified for efficient translation and secretion. Mice that received transplants of IL-15-/- B6 bone marrow cells displayed a significantly longer median survival time (MST) compared with mice that received transplants of wild-type (wt) B6 bone marrow; in contrast, mice that received transplants of IL-15 tg B6 bone marrow cells had a dramatically decreased MST. This decrease in survival was associated with a substantial activation and expansion of effector-memory (CD44highCD62Llow) CD8+ T lymphocytes. Finally, in vivo depletion of either CD4+ or CD8+ T lymphocyte subsets significantly prolonged survival in mice receiving IL-15 tg B6 marrow, while depletion of both CD4+ and CD8+ T cells provided complete protection from acute GVHD. We thus show that acute GVHD is attenuated in the absence of donor bone marrow–derived IL-15 and conclude that donor-derived IL-15 is a critical mediator of T-cell function in acute GVHD.


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