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      Mesenchymal stem cells and immunomodulation: current status and future prospects

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          Abstract

          The unique immunomodulatory properties of mesenchymal stem cells (MSCs) make them an invaluable cell type for the repair of tissue/ organ damage caused by chronic inflammation or autoimmune disorders. Although they hold great promise in the treatment of immune disorders such as graft versus host disease (GvHD) and allergic disorders, there remain many challenges to overcome before their widespread clinical application. An understanding of the biological properties of MSCs will clarify the mechanisms of MSC-based transplantation for immunomodulation. In this review, we summarize the preclinical and clinical studies of MSCs from different adult tissues, discuss the current hurdles to their use and propose the future development of pluripotent stem cell-derived MSCs as an approach to immunomodulation therapy.

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          Treatment of severe acute graft-versus-host disease with third party haploidentical mesenchymal stem cells.

          Katarina Le Blanc, Ida Rasmusson, Berit Sundberg … (2004)
          Adult bone-marrow-derived mesenchymal stem cells are immunosuppressive and prolong the rejection of mismatched skin grafts in animals. We transplanted haploidentical mesenchymal stem cells in a patient with severe treatment-resistant grade IV acute graft-versus-host disease of the gut and liver. Clinical response was striking. The patient is now well after 1 year. We postulate that mesenchymal stem cells have a potent immunosuppressive effect in vivo.
          Article 0 comments Cited 668 times – based on 0 reviews     Review now
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            Mesenchymal stem cells in the Wharton's jelly of the human umbilical cord.

            Hwai-Shi Wang, Shih-Chieh Hung, Shu-Tine Peng … (2004)
            The Wharton's jelly of the umbilical cord contains mucoid connective tissue and fibroblast-like cells. Using flow cytometric analysis, we found that mesenchymal cells isolated from the umbilical cord express matrix receptors (CD44, CD105) and integrin markers (CD29, CD51) but not hematopoietic lineage markers (CD34, CD45). Interestingly, these cells also express significant amounts of mesenchymal stem cell markers (SH2, SH3). We therefore investigated the potential of these cells to differentiate into cardiomyocytes by treating them with 5-azacytidine or by culturing them in cardiomyocyte-conditioned medium and found that both sets of conditions resulted in the expression of cardiomyocyte markers, namely N-cadherin and cardiac troponin I. We also showed that these cells have multilineage potential and that, under suitable culture conditions, are able to differentiate into cells of the adipogenic and osteogenic lineages. These findings may have a significant impact on studies of early human cardiac differentiation, functional genomics, pharmacological testing, cell therapy, and tissue engineering by helping to eliminate worrying ethical and technical issues.
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              Suppression of allogeneic T-cell proliferation by human marrow stromal cells: implications in transplantation.

              William Tse, John Pendleton, Wendy Beyer … (2003)
              Marrow stromal cells (MSC) can differentiate into multiple mesenchymal tissues. To assess the feasibility of human MSC transplantation, we evaluated the in vitro immunogenicity of MSC and their ability to function as alloantigen presenting cells (APC). Human MSC were derived and used in mixed cell cultures with allogeneic peripheral blood mononuclear cells (PBMC). Expression of immunoregulatory molecules on MSC was analyzed by flow cytometry. An MSC-associated suppressive activity was analyzed using cell-proliferation assays and enzyme-linked immunoassays. MSC failed to elicit a proliferative response when cocultured with allogeneic PBMC, despite provision of a costimulatory signal delivered by an anti-CD28 antibody and pretreatment of MSC with gamma-interferon. MSC express major histocompatibility complex (MHC) class I and lymphocyte function-associated antigen (LFA)-3 antigens constitutively and MHC class II and intercellular adhesion molecule (ICAM)-1 antigens upon gamma-interferon treatment but do not express CD80, CD86, or CD40 costimulatory molecules. MSC actively suppressed proliferation of responder PBMC stimulated by third-party allogeneic PBMC as well as T cells stimulated by anti-CD3 and anti-CD28 antibodies. Separation of MSC and PBMC by a semipermeable membrane did not abrogate the suppression. The suppressive activity could not be accounted for by MSC production of interleukin-10, transforming growth factor-beta1, or prostaglandin E2, nor by tryptophan depletion of the culture medium. Human MSC fail to stimulate allogeneic PBMC or T-cell proliferation in mixed cell cultures. Unlike other nonprofessional APC, this failure of function is not reversed by provision of CD28-mediated costimulation nor gamma-interferon pretreatment. Rather, MSC actively inhibit T-cell proliferation, suggesting that allogeneic MSC transplantation might be accomplished without the need for significant host immunosuppression.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cell Death Dis
                Journal ID (iso-abbrev): Cell Death Dis
                Title: Cell Death & Disease
                Publisher: Nature Publishing Group
                ISSN (Electronic): 2041-4889
                Publication date (Print): January 2016
                Publication date (Electronic): 21 January 2016
                Publication date PMC-release: 1 January 2016
                Volume: 7
                Issue: 1
                Page: e2062
                Affiliations
                [1 ]Department of Ophthalmology, Li Ka Shing Faculty of Medicine, The University of Hong Kong , Hong Kong
                [2 ]Department of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong , Hong Kong
                [3 ]Department of Cellular and Molecular Biology, University of Texas Health Science Center at Tyler , Tyler, Texas 75708, USA
                [4 ]Otorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen University , Guangzhou, Guangdong, China
                Author notes
                [* ]Otorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen University , 58 Zhongshan Road II, Guangzhou, Guangdong 510080, China. Tel: +86 13699725962; Fax: +86 020 87333733; E-mail: fuqingl@ 123456mail.sysu.edu.cn
                [* ]Department of Medicine, Department of Ophthalmology, The University of Hong Kong 5 Sassoon Road, Hong Kong. Tel: +852 2831 5403; Fax: +852 2816 2095; E-mail: qzlian@ 123456hku.hk
                [5]

                These authors contributed equally to this work.

                Article
                Publisher Item ID: cddis2015327
                DOI: 10.1038/cddis.2015.327
                PMC ID: 4816164
                PubMed ID: 26794657
                SO-VID: 36c89e76-2461-4438-aba2-b3bf52c0ac12
                Copyright © Copyright © 2016 Macmillan Publishers Limited
                License:

                Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                Date received : 30 July 2015
                Date revision received : 13 September 2015
                Date accepted : 25 September 2015
                Categories
                Subject: Review

                ScienceOpen disciplines: Cell biology
                Data availability:
                ScienceOpen disciplines: Cell biology

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