Different mechanisms causing loss of mismatched human leukocyte antigens in relapsing t(6;11)(q27;q23) acute myeloid leukemia after haploidentical transplantation

Eur J Haematol. 2012 Dec;89(6):497-500. doi: 10.1111/ejh.12017. Epub 2012 Oct 26.

Abstract

Mismatched human leukocyte antigens (HLAs) on leukemic cells can be targeted by donor T cells in HLA-mismatched/haploidentical stem cell transplantation. In two cases of acute myeloid leukemia with t(6;11)(q27;q23) abnormality presented here, flow cytometry analysis showed a lack of HLA-A unshared between recipients and donors in relapsing leukemic cells after HLA-haploidentical transplantation. However, high-resolution HLA genotyping showed that one case lacked a corresponding HLA haplotype, whereas the other preserved it. These cases suggest that leukemic cells, which lacked mismatched HLA expression, might have an advantage in selective expansion under donor T-cell immune surveillance after HLA-haploidentical transplantation. Most importantly, down-regulation of unshared HLA expression potentially occurs by genetic alterations other than loss of HLA alleles.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Bone Marrow Transplantation*
  • Chromosomes, Human, Pair 11 / immunology
  • Chromosomes, Human, Pair 6 / immunology
  • Female
  • Graft vs Host Disease / genetics
  • HLA Antigens / genetics*
  • HLA Antigens / immunology
  • Haplotypes
  • Hematopoietic Stem Cell Transplantation*
  • Histocompatibility
  • Histocompatibility Testing
  • Humans
  • Leukemia, Myeloid, Acute / genetics*
  • Leukemia, Myeloid, Acute / immunology
  • Recurrence
  • T-Lymphocytes / immunology
  • Tissue Donors
  • Translocation, Genetic / immunology
  • Transplantation, Homologous

Substances

  • HLA Antigens