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Ann Hematol. 2022 Jan 18; doi: 10.1007/s00277-022-04757-3. Epub 2022 Jan 18.

HLA-G-ILT2 interaction contributes to suppression of bone marrow B cell proliferation in acquired aplastic anemia.

Annals of hematology

Yuan-Xin Sun, Qi Feng, Shu-Wen Wang, Xin Li, Zi Sheng, Jun Peng

Affiliations

  1. Department of Hemodialysis, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
  2. Department of Hematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
  3. Shandong Provincial Key Laboratory of Immunohematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
  4. Department of Hematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China. [email protected].
  5. School of Medicine, Cheeloo College of Medicine, Shandong University, Jinan, China. [email protected].
  6. Department of Hematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China. [email protected].
  7. State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Disease Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China. [email protected].

PMID: 35041051 DOI: 10.1007/s00277-022-04757-3

Abstract

Acquired aplastic anemia (AA) is an autoimmune disease characterized by hematopoietic stem and progenitor cell destruction in bone marrow. The non-classic human leukocyte class I antigen (HLA-) G interacts with multiple cell subsets, such as T cells and B cells. HLA-G exerts powerful immune suppression by binding with its receptors, immunoglobulin-like transcripts (ILTs). Here, we compared 46 AA patients and 28 healthy controls. Soluble HLA-G levels in bone marrow supernatants from AA patients were higher than controls. The proportion of bone marrow B cells was decreased and the ILT2-expressing cells among CD19

© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

Keywords: Aplastic anemia; Bone marrow B cells; HLA-G; ILT2

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