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Blood, 15 January 2008, Vol. 111, No. 2, pp. 534-536.
Prepublished online as a Blood First Edition Paper on October 23, 2007; DOI 10.1182/blood-2007-05-090928.
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Submitted May 16, 2007
Accepted September 28, 2007
Polymorphisms in the chemokine (C-X-C motif) ligand 10 are associated with invasive aspergillosis after allogeneic stem cell transplantation and influence CXCL10 expression in monocyte-derived dendritic cells
Markus Mezger, Michael Steffens, Melanie Beyer, Carolin Manger, Johannes Eberle, Mohammad-Reza Toliat, Thomas F Wienker, Per Ljungman, Holger Hebart, Hans Jurgen Dornbusch, Hermann Einsele, and Juergen Loeffler*
Medizinische Klinik und Poliklinik II, Julius-Maximilians-Universitat, Wurzburg, Germany
Institut fur Medizinische Biometrie, Informatik und Epidemiologie der Rheinische Friedrich-Wilhelms-Universitat, Bonn, Germany
Cologne Centre for Genomics, Koln, Germany
Karolinska University Hospital, Stockholm, Sweden
Medizinische Klinik II, Universitatsklinikum Tubingen, Tubingen, Germany
Universitatetsklinik fur Kinder- & Jugendheilkunde, Graz, Austria
* Corresponding author; email: loeffler_j{at}klinik.uni-wuerzburg.de.
Patients after allogeneic stem cell transplantation (alloSCT) have an increased risk for invasive aspergillosis (IA). Here, recipients of an allograft with IA (n = 81) or without IA (n =58) were screened for 84 single nucleotide polymorphisms in 18 immune relevant genes.
We found three markers in chemokine (C-X-C motif) ligand 10 (CXCL10, 4q21, 11101 C>T, p=0.007; 1642 C<G, p=0.003; -1101 A<G, p=0.001) significantly associated with an increased risk of developing IA. Furthermore, immature dendritic cells (iDCs) exposed to Aspergillus fumigatus germlings showed markedly higher CXCL10 expression, if carrying the wild type genotype compared to the "CGAG" high risk haplotype. In addition, serum from patients with proven / probable IA showed increased serum levels of CXCL10, compared to immunocompromised patients without IA. Thus, polymorphisms in CXCL10 determine chemokine secretion by iDCs upon exposure to A. fumigatus and most likely thereby genetically determine the risk of IA after alloSCT.
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