Blood, 15 October 2004, Vol.
104, No. 8, pp. 2425-2431.
Prepublished
online as a Blood First Edition Paper on June 24, 2004; DOI
10.1182/blood-2004-05-1839.
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IMMUNOBIOLOGY
Diazepam-binding inhibitor-related protein 1: a candidate
autoantigen in acquired aplastic anemia patients harboring a minor
population of paroxysmal nocturnal hemoglobinuria–type cells
Xingmin Feng, Tatsuya
Chuhjo, Chiharu Sugimori, Takeharu
Kotani, Xuzhang Lu, Akiyoshi
Takami, Hiroyuki Takamatsu, Hirohito
Yamazaki, and Shinji Nakao
From the Cellular Transplantation Biology, Kanazawa University
Graduate School of Medical Science, Ishikawa, Japan; and the
Protected Environmental Unit, Kanazawa University Hospital,
Kanazawa, Ishikawa, Japan.
To identify candidate antigens in aplastic anemia
(AA), we screened proteins derived from a leukemia cell
line with serum of an AA patient and identified
diazepam-binding inhibitor-related protein 1 (DRS-1).
Enzyme-linked immunosorbent assay (ELISA) revealed high
titers of anti–DRS-1 antibodies (DRS-1 Abs) in 27 (38.0%)
of 71 AA patients displaying increased paroxysmal
nocturnal hemoglobinuria (PNH)–type cells (PNH+), 2
(6.3%) of 32 PNH– AA patients, 5 (38.5%) of 13
PNH+ myelodysplastic syndrome (MDS) patients,
and none of 42 PNH– MDS patients. DRS-1 gene
was abundantly expressed in myeloid leukemia cell lines
and in CD34+ cells derived from healthy individuals.
Stimulation of T cells from an AA patient displaying high
DRS-1 Abs with a putative CD4+ T-cell epitope
(amino acid residues [aa's] 191-204) presented by
HLA-DR15, which overlapped with a hot spot (aa's 173-198)
of DRS-1 Ab epitopes, gave rise to T cells cytotoxic for
L cells (murine fibroblasts) that were transfected with
DRB1*1501 and DRS-1. Enzyme-linked immunospot assay
demonstrated increased frequency of T-cell precursors
specific to the DRS-1 peptide in other
HLA-DR15+ AA patients displaying high DRS-1 Ab
titers. These findings indicate that DRS-1 may serve as an
autoantigen eliciting immune attack against hematopoietic
stem cells in a subset of AA patients characterized by
increased PNH-type cells.
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