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Blood, 1 August 2004, Vol. 104, No. 3, pp. 889-894.
Prepublished online as a Blood First Edition Paper on April 15, 2004; DOI 10.1182/blood-2003-10-3543.
 Previous Article | Table of Contents | Next Article 
TRANSPLANTATION
Both donor and recipient NOD2/CARD15 mutations associate with transplant-related mortality and GvHD following allogeneic stem cell transplantation
Ernst Holler,
Gerhard Rogler,
Hans Herfarth,
Julia Brenmoehl,
Peter Johannes Wild,
Joachim Hahn,
Günther Eissner,
Jürgen Schölmerich, and
Reinhard Andreesen
From the Division of Hematology/Oncology, the Department of Internal Medicine I, and the Institute of Pathology, University Hospital of Regensburg, Germany.
Single nucleotide polymorphisms (SNPs) of the NOD2/CARD15 gene resulting in a diminished nuclear factor- B (NF-B) response to bacterial cell wall products have been associated with an increased incidence of Crohn disease. To assess a possible contribution of NOD2/CARD15 mutations to graft-versus-host disease (GvHD) and complications following allogeneic stem cell transplantation, we retrospectively typed DNA from donor/recipient pairs in 169 consecutive patients receiving transplants from related or unrelated donors. Mutated alleles were observed in 21% of patients and in 14% of donors. Cumulative incidence of 1-year, transplant-related mortality rose from 20% in donor/recipient pairs without mutated SNPs to 49% in pairs with recipient mutations (P = .03) and 59% in pairs with donor mutations (P < .005), and was highest in 12 pairs with mutated alleles in both donor and recipients (83%; P < .001). Similar associations were observed for severe overall and severe gastrointestinal GvHD. The impact of NOD2/CARD15 mutations was more prominent for HLA-identical sibling transplantations but was also observed in unrelated donor transplantation. Mutations proved to be independent risk factors for transplant-related mortality. Our findings indicate a major role of monocyte/macrophage dysfunction in the pathophysiology of GvHD and strongly suggest a future risk assessment or even donor selection through NOD2/CARD15 typing.
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