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Reply to Verheyden and Demanet

Leukemia volume 22, page 2131 (2008)Cite this article

Dr Verheyden and Dr Demanet1 raised several interesting questions in their comment to our letter.2 Following their suggestion, we additionally analyzed chronic myelogenous leukemia (CML) patients and their donors with regard to homozygosity for haplotype A and killer immunoglobuline-like receptor (KIR)1D to identify subjects lacking any functional activating KIR. In the respective groups, the frequencies were 25.8 and 16.1%. As this difference was not statistically significant, it may be hypothesized that the effect of activating KIRs is rather qualitative and restricted to KIR2DS4 while other activating KIRs do not appear to play a role. Indeed, the frequencies of KIR2DS1, KIR2DS2, KIR2DS3, KIR2DS5, and KIR3DS1 were similar among CML patients and their donors. As well, the median sum of all activating KIRs was comparable (data not shown).

In our study, we used human leukocyte antigen (HLA)-matched bone marrow donors as a representative control group, considering that (i) HLA genotype is associated with the occurrence and the age-at-onset of CML3, 4 and (ii) KIR–HLA ligand interactions appear to play a role in the pathogenesis of leukemia.5 HLA-identical siblings constituted 32.3% of donors in a cohort of CML, 36.8% in acute myeloid leukemia and 33.3% in acute lymphoblastic leukemia (P=NS). However, as suggested by Verheyden and Demanet,1 we additionally looked at data available for the Polish population (I Nowak, E Majorczyk, P Kusnierczyk, unpublished data). Among 363 healthy individuals, 63.2% were KIR2DS4*001−/KIR1D+ compared to 77.4% in our CML cohort (P=0.08).

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References

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Authors and Affiliations

  1. Department of Hematology and Bone Marrow Transplantation, Silesian Medical University, Katowice, Poland

    S Giebel

  2. Department of Clinical Immunology, Laboratory of Immunogenetics, Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland

    I Nowak, E Majorczyk & P Kusnierczyk

  3. Department of Microbiology and Biotechnology, Faculty of Natural Sciences, Institute of Chemistry and Environmental Sciences, Jan Dlugosz Pedagogical University, Czestochowa, Poland

    P Kusnierczyk

Authors
  1. S Giebel
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  2. I Nowak
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  3. E Majorczyk
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  4. P Kusnierczyk
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Correspondence to S Giebel.

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Giebel, S., Nowak, I., Majorczyk, E. et al. Reply to Verheyden and Demanet. Leukemia 22, 2131 (2008). https://doi.org/10.1038/leu.2008.110

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