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Frequent loss of HLA alleles associated with copy number-neutral 6pLOH in acquired aplastic anemia
http://hdl.handle.net/2297/30143
http://hdl.handle.net/2297/30143be6a3ba9-77af-4b03-9739-4059045e01d1
| 名前 / ファイル | ライセンス | アクション |
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ME-PR-KATAGIRI-T-Supplementary Information.pdf (4.7 MB)
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ME-PR-KATAGIRI-T-6601.pdf (1.1 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2017-10-03 | |||||
| タイトル | ||||||
| タイトル | Frequent loss of HLA alleles associated with copy number-neutral 6pLOH in acquired aplastic anemia | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| 著者 |
Katagiri, Takamasa
× Katagiri, Takamasa× Sato-Otsubo, Aiko× Kashiwase, Koichi× Morishima, Satoko× Sato, Yusuke× Mori, Yuka× Kato, Motohiro× Sanada, Masashi× Morishima, Yasuo× Hosokawa, Kohei× Sasaki, Yumi× Ohtake, Shigeki× Ogawa, Seishi× Nakao, Shinji |
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| 書誌情報 |
Blood 巻 118, 号 25, p. 6601-6609, 発行日 2011-12-15 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0006-4971 | |||||
| NCID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA00567156 | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1182/blood-2011-07-365189 | |||||
| 出版者 | ||||||
| 出版者 | American Society of Hematology | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Idiopathic aplastic anemia (AA) is a common cause of acquired BM failure. Although autoimmunity to hematopoietic progenitors is thought to be responsible for its pathogenesis, little is known about the molecular basis of this autoimmunity. Here we show that a substantial proportion of AA patients harbor clonal hematopoiesis characterized by the presence of acquired copy number-neutral loss of heterozygosity (CNN-LOH) of the 6p arms (6pLOH). The 6pLOH commonly involved the HLA locus, leading to loss of one HLA haplotype. Loss of HLA-Aexpression from multiple lineages of leukocytes was confirmed by flow cytometry in all 6pLOH(+) cases. Surprisingly, the missing HLAalleles in 6pLOH(+) clones were conspicuously biased to particular alleles, including HLA-A*02:01, A*02:06, A*31:01, and B*40:02. A large-scale epidemiologic study on the HLA alleles of patients with various hematologic diseases revealed that the 4 HLA alleles were over-represented in the germline of AA patients. These findings indicate that the 6pLOH(+) hematopoiesis found in AA represents "escapes"hematopoiesis from the autoimmunity, which is mediated by cytotoxic T cells that target the relevant autoantigens presented on hematopoietic progenitors through these class I HLAs. Our results provide a novel insight into the genetic basis of the pathogenesis of AA. © 2011 by The American Society of Hematology. | |||||
| 著者版フラグ | ||||||
| 出版タイプ | AM | |||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
