@article{oai:kanazawa-u.repo.nii.ac.jp:00014027,
 author = {Maruyama, Hiroyuki and Katagiri, Takamasa and Kashiwase, Koichi and Shiina, Takashi and Sato-Otsubo, Aiko and Zaimoku, Yoshitaka and Maruyama, Kana and Hosokawa, Kohei and Ishiyama, Ken and Yamazaki, Hirohito and Inoko, Hidetoshi and Ogawa, Seishi and Nakao, Shinji},
 issue = {10},
 journal = {Experimental Hematology},
 month = {Oct},
 note = {To gain insight into the origin and clinical significance of leukocytes that lack human leukocyte antigen A (HLA-A) allele expression caused by a copy-number-neutral loss of heterozygosity in the short arm of chromosome 6 in patients with acquired aplastic anemia (AA), we used a high-sensitivity flow cytometry assay to investigate the presence of HLA-A allele-lacking leukocytes (HLA-LLs) in 144 AA patients. HLA-LLs, accounting for 0.2–99.8% of each leukocyte population, were detected in 18 of 71 (25.4%) newly diagnosed patients and in 25 of 73 (34.2%) previously treated patients. The lineage combination patterns of the HLA-LLs in the 43 HLA-LL+ patients were granulocytes (Gs), monocytes (Ms), B cells (Bs), and T cells (Ts; GMBT) in 13 cases, GMB in 16 cases, GM in 11 cases, and B alone in three cases. The response rate to antithymocyte globulin plus cyclosporine therapy (100%) and the 2-year, failure-free survival rate (100%) in 8 newly diagnosed HLA-LL+ patients were significantly higher than in 23 HLA-LL− patients (52.2% for both). These data suggest that HLA-LLs are a useful marker of the presence of immune pathophysiology in AA and that T-cell attacks against hematopoietic progenitor cells, rather than against hematopoietic stem cells, can trigger bone marrow failure in AA patients. © 2016 ISEH - International Society for Experimental Hematology, Embargo Period 12 months},
 pages = {931--939.e3},
 title = {Clinical significance and origin of leukocytes that lack HLA-A allele expression in patients with acquired aplastic anemia},
 volume = {44},
 year = {2016}
}