The plasticity of mesenchymal stem cells in regulating surface HLA-I

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Wang , Y , Huang , J , Gong , L , Yu , D , An , C , Bunpetch , V , Dai , J , Huang , H , Zou , X , Ouyang , H & Liu , H 2019 , ' The plasticity of mesenchymal stem cells in regulating surface HLA-I ' , iScience , vol. 15 , pp. 66-+ .

Title: The plasticity of mesenchymal stem cells in regulating surface HLA-I
Author: Wang, Yafei; Huang, Jiayun; Gong, Lin; Yu, Dongsheng; An, Chenrui; Bunpetch, Varitsara; Dai, Jun; Huang, He; Zou, Xiaohui; Ouyang, Hongwei; Liu, Hua
Contributor organization: Research Program in Systems Oncology
Department of Medical and Clinical Genetics
University of Helsinki
Date: 2019-05-31
Language: eng
Number of pages: 28
Belongs to series: iScience
ISSN: 2589-0042
Abstract: Summary A low surface expression level of human leukocyte antigen class I(HLA-I) ensures the mesenchymal stem cells’(MSCs) escape from the allogeneic recipients’ immunological surveillance. Here, we discovered that both transcriptional and synthesis levels of HLA-I in MSCs increased continuously after IFN-γ treatment, while interestingly, their surface HLA-I expression was downregulated after reaching an HLA-I surface expression peak. Microarray data indicated the post-transcriptional process plays an important role in downregulation of surface HLA-I. Further studies identified that IFN-γ-treated MSCs accelerated HLA-I endocytosis through a Clathrin–independent Dynamin-dependent endocytosis pathway. Furthermore, the cells which have self-downregulated surface HLA-I expression elicit a weaker immune response than they previously could. Thus, uncovering the plasticity of MSCs in the regulation of HLA-I surface expression would reveal insights into the membrane-transportation events leading to the maintenance of low surface HLA-I expression, providing more evidence for selecting and optimizing low immunogenic MSCs to improve the therapeutic efficiency.
3111 Biomedicine
Peer reviewed: Yes
Rights: cc_by_nc_nd
Usage restriction: openAccess
Self-archived version: acceptedVersion

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