期刊
EXPERIMENTAL HEMATOLOGY
卷 36, 期 11, 页码 1545-1555出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.exphem.2008.06.008
关键词
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资金
- Committee on Research and Conference Grants (CRCG)
- The University of Hong Kong
- S.K. Ho-Tung Charitable Fund
Objective. Under the influence of interferon-gamma (IFN-gamma), mesenchymal stromal cells (MSCs) are conditional antigen-presenting cells, which have immunosuppressive potential. Apart from IFN-gamma upregulation of major histocompatibility complexes class I and II (MHC-I and MHC-II) expression, the underlying kinetics and mechanisms have not been described previously. This information is helpful to delineate how human MSCs can be modulated by IFN-gamma in different clinical scenarios. Materials and Methods. Here, we demonstrated that IFN-gamma-treated MSCs underwent classical signal transduction pathway via phosphorylation of signal transducers and activators of transcription-1, activation of interferon regulatory factor-1, and class II transactivator comparable to that of primary human blood macrophages. Results. IFN-gamma markedly induced expression of MHC-I instantly, while its effects on MHC-II were less dramatic and delayed up to 4 days. This is due to a slower intracellular transport of the MHC-II antigen to the membrane surface. More important is that MSCs showed a reduction in their proliferation by 50% without evidence of cell death after prolonged IFN-gamma treatment for 8 days. High-dose IFN-gamma-treated MSCs (500 U/mL) could initiate T-cell activation as indicated by expression of CD25 and proliferation of allogeneic T cells. Conclusions. The summative IFN-gamma effects will adversely affect the immunoprivilege status and lifespan of MSCs. (c) 2008 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc.
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