Attapon Cheepsattayakorn1*, Ruangrong
Cheepsattayakorn2
1-10th Zonal Tuberculosis and Chest
Disease Center, Chiang Mai, Thailand
2- Department of Pathology, Faculty
of Medicine, Chiang Mai University, Chiang Mai, Thailand
*Corresponding Author: Attapon
Cheepsattayakorn, 10th Zonal Tuberculosis and Chest Disease Center, 143
Sridornchai Road Changklan Muang Chiang Mai 50100, Thailand. Tel: +66 53140767;
+66 53276364; Email: [email protected]
Published Date: 10-04-2020
Copyright© 2020 by Cheepsattayakorn
A, et al. All rights reserved. This is an open access article distributed under
the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the
original author and source are credited.
Editorial
In-vitro, Mesenchymal Stem Cell (MSC)
populations with potentials of similar multi-lineage differentiation have been
obtained from several Bone Marrow (BM) and non-bone marrow tissues, including
umbilical cord, placenta, amniotic fluid, adipose tissue, and peripheral blood
[1-10]. The clonogenic BM-human MSCs fraction ranges from 10 to 100
Colony-Forming Unit-Fibroblast (CFU-F) per 106 Marrow Mononuclear Cells (MNCs)
[11]. BM-human MCSs are characterized by lacking CD11b, CD14, CD19, D34, CD45,
CD79α, and Human Leukocyte Antigen (HLA)-DR expression; positive expression of
surface antigens CD73, CD90, and CD105; multipotency (i.e., chondrogenic,
osteogenic, and adipogenic); and their adherence to plastic [11]. By the year
2000, clinicians increasingly had become interested in intravenously applied
MSC therapy [12]. A previous study demonstrated that both human and murine MCSs
can induce immune suppression by attracting and killing auto reactive T cells
via FasL, therefore stimulating Transforming Growth Factor-beta (TGF-β)
production by macrophages and generation of regulatory T cells [13]. The dying
T cells that is caused by the interaction involving the MSC-induced Monocyte
Chemoattractant Protein-1 (MCP-1) secretion in turn activate macrophages to
produce TGF-β, then stimulating regulatory T cells and promoting immune
tolerance [14]. The capacity of MSCs for in-vivo differentiation and
engraftment and by their efficacy in promoting wound healing highlighted its
clinical relevance [15-21].
In 2006, the International Society
for Cellular Therapy came up with the guidelines for MSC characterization for
standardization the MSC biology, definition, isolation, and characterization
criteria, in-vivo relevance, and ethical and institutional regulations for
its clinical use [11]. Since the COVID-19 pandemic, there are several
ongoing trials that have been studied in China, such as the ClinicalYtrials.gov
identifiers: NCT04252118, NCT04273646, NCT04276987, NCT04293692, NCT04302519, NCT04288102,
etc. for fighting against severe COVID-19 or COVID-19 pneumonia [22-27]. MSCs
can decrease the overproduction of immune cells caused by a reaction to the
COVID-19 and decrease excessive levels of inflammatory substances, contributing
to regulating the immune system and recovering to the normal status,
particularly of the elderly patients [28].
In conclusion, human MSCs are
currently being evaluated as a stem cell treatment for a number of diseases,
particularly severe COVID-19 and have been demonstrated to be safe in clinical
trials. Nevertheless, further studies are urgently needed to investigate and
optimize a number of variables in the human MSC culture environment by
developing a bioprocess that can be operated in accordance with the Good
Manufacturing Product (GMP).
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Article Type
Editorial
Publication History
Received Date: 01-04-2020
Accepted Date: 03-04-2020
Published Date: 10-04-2020
Copyright© 2020 by Cheepsattayakorn A, et al. All rights reserved. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Citation: Cheepsattayakorn A, Cheepsattayakorn R. Mesenchymal Stem Cell Transplantation for COVID-19. J Clin Immunol Microbiol. 2020; 1 (1):1-4.