Mesenchymal Stem Cells: Allogeneic MSC May Be Immunosuppressive but Autologous MSC Are Dysfunctional in Lupus Patients
Identifieur interne : 000C78 ( Ncbi/Merge ); précédent : 000C77; suivant : 000C79Mesenchymal Stem Cells: Allogeneic MSC May Be Immunosuppressive but Autologous MSC Are Dysfunctional in Lupus Patients
Auteurs : Rui-Juan Cheng [République populaire de Chine] ; An-Ji Xiong [République populaire de Chine] ; Yan-Hong Li [République populaire de Chine] ; Shu-Yue Pan [République populaire de Chine] ; Qiu-Ping Zhang [République populaire de Chine] ; Yi Zhao [République populaire de Chine] ; Yi Liu [République populaire de Chine] ; Tony N. Marion [République populaire de Chine, États-Unis]Source :
- Frontiers in Cell and Developmental Biology [ 2296-634X ] ; 2019.
Abstract
Mesenchymal stem cells (MSCs) have a potently immunosuppressive capacity in both innate and adaptive immune responses. Consequently, MSCs transplantation has emerged as a potential beneficial therapy for autoimmune diseases even though the mechanisms underlying the immunomodulatory activity of MSCs is incompletely understood. Transplanted MSCs from healthy individuals with no known history of autoimmune disease are immunosuppressive in systemic lupus erythematosus (SLE) patients and can ameliorate SLE disease symptoms in those same patients. In contrast, autologous MSCs from SLE patients are not immunosuppressive and do not ameliorate disease symptoms. Recent studies have shown that MSCs from SLE patients are dysfunctional in both proliferation and immunoregulation and phenotypically senescent. The senescent phenotype has been attributed to multiple genes and signaling pathways. In this review, we focus on the possible mechanisms for the defective phenotype and function of MSCs from SLE patients and summarize recent research on MSCs in autoimmune diseases.
Url:
DOI: 10.3389/fcell.2019.00285
PubMed: 31799252
PubMed Central: 6874144
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<front><div type="abstract" xml:lang="en"><p>Mesenchymal stem cells (MSCs) have a potently immunosuppressive capacity in both innate and adaptive immune responses. Consequently, MSCs transplantation has emerged as a potential beneficial therapy for autoimmune diseases even though the mechanisms underlying the immunomodulatory activity of MSCs is incompletely understood. Transplanted MSCs from healthy individuals with no known history of autoimmune disease are immunosuppressive in systemic lupus erythematosus (SLE) patients and can ameliorate SLE disease symptoms in those same patients. In contrast, autologous MSCs from SLE patients are not immunosuppressive and do not ameliorate disease symptoms. Recent studies have shown that MSCs from SLE patients are dysfunctional in both proliferation and immunoregulation and phenotypically senescent. The senescent phenotype has been attributed to multiple genes and signaling pathways. In this review, we focus on the possible mechanisms for the defective phenotype and function of MSCs from SLE patients and summarize recent research on MSCs in autoimmune diseases.</p>
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Cell Dev Biol</journal-id>
<journal-id journal-id-type="iso-abbrev">Front Cell Dev Biol</journal-id>
<journal-id journal-id-type="publisher-id">Front. Cell Dev. Biol.</journal-id>
<journal-title-group><journal-title>Frontiers in Cell and Developmental Biology</journal-title>
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<issn pub-type="epub">2296-634X</issn>
<publisher><publisher-name>Frontiers Media S.A.</publisher-name>
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</journal-meta>
<article-meta><article-id pub-id-type="pmid">31799252</article-id>
<article-id pub-id-type="pmc">6874144</article-id>
<article-id pub-id-type="doi">10.3389/fcell.2019.00285</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Cell and Developmental Biology</subject>
<subj-group><subject>Review</subject>
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</subj-group>
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<title-group><article-title>Mesenchymal Stem Cells: Allogeneic MSC May Be Immunosuppressive but Autologous MSC Are Dysfunctional in Lupus Patients</article-title>
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<xref ref-type="aff" rid="aff1"><sup>1</sup>
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<aff id="aff1"><sup>1</sup>
<institution>Department of Rheumatology and Immunology, West China Hospital, Sichuan University</institution>
,<addr-line>Chengdu</addr-line>
,<country>China</country>
</aff>
<aff id="aff2"><sup>2</sup>
<institution>Department of Rheumatology and Immunology, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College</institution>
,<addr-line>Nanchong</addr-line>
,<country>China</country>
</aff>
<aff id="aff3"><sup>3</sup>
<institution>Department of Microbiology, Immunology, and Biochemistry, University of Tennessee Health Science Center</institution>
,<addr-line>Memphis, TN</addr-line>
,<country>United States</country>
</aff>
<author-notes><fn fn-type="edited-by"><p>Edited by: Gianluca Carnevale, University of Modena and Reggio Emilia, Italy</p>
</fn>
<fn fn-type="edited-by"><p>Reviewed by: Gianandrea Pasquinelli, University of Bologna, Italy; Philippe Bourin, Independent Researcher, France</p>
</fn>
<corresp id="c001">*Correspondence: Yi Liu, <email>yi2006liu@163.com</email>
</corresp>
<fn fn-type="other" id="fn004"><p>This article was submitted to Stem Cell Research, a section of the journal Frontiers in Cell and Developmental Biology</p>
</fn>
</author-notes>
<pub-date pub-type="epub"><day>15</day>
<month>11</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="collection"><year>2019</year>
</pub-date>
<volume>7</volume>
<elocation-id>285</elocation-id>
<history><date date-type="received"><day>13</day>
<month>9</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>04</day>
<month>11</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2019 Cheng, Xiong, Li, Pan, Zhang, Zhao, Liu and Marion.</copyright-statement>
<copyright-year>2019</copyright-year>
<copyright-holder>Cheng, Xiong, Li, Pan, Zhang, Zhao, Liu and Marion</copyright-holder>
<license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</license-p>
</license>
</permissions>
<abstract><p>Mesenchymal stem cells (MSCs) have a potently immunosuppressive capacity in both innate and adaptive immune responses. Consequently, MSCs transplantation has emerged as a potential beneficial therapy for autoimmune diseases even though the mechanisms underlying the immunomodulatory activity of MSCs is incompletely understood. Transplanted MSCs from healthy individuals with no known history of autoimmune disease are immunosuppressive in systemic lupus erythematosus (SLE) patients and can ameliorate SLE disease symptoms in those same patients. In contrast, autologous MSCs from SLE patients are not immunosuppressive and do not ameliorate disease symptoms. Recent studies have shown that MSCs from SLE patients are dysfunctional in both proliferation and immunoregulation and phenotypically senescent. The senescent phenotype has been attributed to multiple genes and signaling pathways. In this review, we focus on the possible mechanisms for the defective phenotype and function of MSCs from SLE patients and summarize recent research on MSCs in autoimmune diseases.</p>
</abstract>
<kwd-group><kwd>systemic lupus erythematosus</kwd>
<kwd>mesenchymal stem cells</kwd>
<kwd>dysfunction</kwd>
<kwd>senescence</kwd>
<kwd>immunoregulatory</kwd>
</kwd-group>
<funding-group><award-group><funding-source id="cn001">Department of Science and Technology of Sichuan Province<named-content content-type="fundref-id">10.13039/501100004829</named-content>
</funding-source>
<award-id rid="cn001">2019YJ0099</award-id>
</award-group>
</funding-group>
<counts><fig-count count="3"></fig-count>
<table-count count="0"></table-count>
<equation-count count="0"></equation-count>
<ref-count count="136"></ref-count>
<page-count count="13"></page-count>
<word-count count="0"></word-count>
</counts>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>République populaire de Chine</li>
<li>États-Unis</li>
</country>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Cheng, Rui Juan" sort="Cheng, Rui Juan" uniqKey="Cheng R" first="Rui-Juan" last="Cheng">Rui-Juan Cheng</name>
</noRegion>
<name sortKey="Li, Yan Hong" sort="Li, Yan Hong" uniqKey="Li Y" first="Yan-Hong" last="Li">Yan-Hong Li</name>
<name sortKey="Liu, Yi" sort="Liu, Yi" uniqKey="Liu Y" first="Yi" last="Liu">Yi Liu</name>
<name sortKey="Marion, Tony N" sort="Marion, Tony N" uniqKey="Marion T" first="Tony N." last="Marion">Tony N. Marion</name>
<name sortKey="Pan, Shu Yue" sort="Pan, Shu Yue" uniqKey="Pan S" first="Shu-Yue" last="Pan">Shu-Yue Pan</name>
<name sortKey="Xiong, An Ji" sort="Xiong, An Ji" uniqKey="Xiong A" first="An-Ji" last="Xiong">An-Ji Xiong</name>
<name sortKey="Zhang, Qiu Ping" sort="Zhang, Qiu Ping" uniqKey="Zhang Q" first="Qiu-Ping" last="Zhang">Qiu-Ping Zhang</name>
<name sortKey="Zhao, Yi" sort="Zhao, Yi" uniqKey="Zhao Y" first="Yi" last="Zhao">Yi Zhao</name>
</country>
<country name="États-Unis"><noRegion><name sortKey="Marion, Tony N" sort="Marion, Tony N" uniqKey="Marion T" first="Tony N." last="Marion">Tony N. Marion</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>
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