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World J Stem Cells. Dec 26, 2017; 9(12): 219-226
Published online Dec 26, 2017. doi: 10.4252/wjsc.v9.i12.219
Yin and Yang of mesenchymal stem cells and aplastic anemia
Larisa Broglie, David Margolis, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI 53226, United States
Jeffrey A Medin, Departments of Pediatrics and Biochemistry, Medical College of Wisconsin, Milwaukee, WI 53226, United States
ORCID number: Larisa Broglie (0000-0002-1674-048X); David Margolis (0000-0001-7608-3058); Jeffrey A Medin (0000-0001-8165-8995).
Author contributions: All authors contributed to the conception and design of the study; Broglie L performed the literature review and wrote the initial draft; Margolis D and Medin JA were involved in critical revision and editing; all authors approved the final version of the manuscript.
Supported by National Center for Advancing Translational Sciences, National Institutes of Health, through Grant Nos. UL1TR001436 and 1TL1TR001437 (to Broglie L); and MACC Fund (to Margolis D and Medin JA). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH.
Conflict-of-interest statement: The authors declare that they have no conflicts of interest with this work.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Correspondence to: Larisa Broglie, MD, Academic Fellow, Instructor, Department of Pediatrics, Medical College of Wisconsin, 8701 Watertown Plank Rd, MFRC 3018, Milwaukee, WI 53226, United States.
Telephone: +1-414-2664122 Fax: +1-414-9556543
Received: August 1, 2017
Peer-review started: August 3, 2017
First decision: September 4, 2017
Revised: September 14, 2017
Accepted: October 17, 2017
Article in press: October 17, 2017
Published online: December 26, 2017


Acquired aplastic anemia (AA) is a bone marrow failure syndrome characterized by peripheral cytopenias and bone marrow hypoplasia. It is ultimately fatal without treatment, most commonly from infection or hemorrhage. Current treatments focus on suppressing immune-mediated destruction of bone marrow stem cells or replacing hematopoietic stem cells (HSCs) by transplantation. Our incomplete understanding of the pathogenesis of AA has limited development of targeted treatment options. Mesenchymal stem cells (MSCs) play a vital role in HSC proliferation; they also modulate immune responses and maintain an environment supportive of hematopoiesis. Some of the observed clinical manifestations of AA can be explained by mesenchymal dysfunction. MSC infusions have been shown to be safe and may offer new approaches for the treatment of this disorder. Indeed, infusions of MSCs may help suppress auto-reactive, T-cell mediated HSC destruction and help restore an environment that supports hematopoiesis. Small pilot studies using MSCs as monotherapy or as adjuncts to HSC transplantation have been attempted as treatments for AA. Here we review the current understanding of the pathogenesis of AA and the function of MSCs, and suggest that MSCs should be a target for further research and clinical trials in this disorder.

Key Words: Hematopoiesis, Targeted therapies, Stem cells, Hematopoietic stem cell transplantation, Aplastic anemia, Mesenchymal stem cells

Core tip: Acquired aplastic anemia (AA) is a bone marrow failure syndrome characterized by peripheral cytopenia and bone marrow hypoplasia and is ultimately fatal without treatment. Our incomplete understanding of the pathogenesis of AA has limited development of targeted treatment options. Here we review the current understanding of the pathogenesis of AA and the function of mesenchymal stem cells (MSCs), and suggest that MSCs should be a target for further trials in AA.


Aplastic anemia (AA) is an acquired bone marrow failure syndrome characterized by pancytopenia and bone marrow hypoplasia. Patients often become dependent on blood and platelet transfusions and are at risk for significant infections from neutropenia and leukopenia. The natural history of untreated AA is death, most commonly from infection or hemorrhage. Current treatments focus on suppressing immune-mediated destruction of bone marrow stem cells or replacing hematopoietic stem cells (HSCs) by transplantation. However, our incomplete understanding of the pathogenesis of AA has limited development of targeted treatment options. Here we review the current understanding of the pathogenesis of AA and the role that mesenchymal stem cells (MSCs) can play in treatment.


Patients with AA enter medical care after presenting with symptoms related to pancytopenia - fatigue from anemia, bleeding from thrombocytopenia, or infection from neutropenia. The diagnostic criteria for AA include cytopenias and decreased marrow cellularity as noted in Table 1[1]. Congenital bone marrow failure syndromes such as Fanconi Anemia and Dyskeratosis Congenita can present similarly. However bone marrow failure syndromes such as these can be identified by disease-specific genetic testing that is often performed as part of the initial evaluation of AA. When a genetic mutation is identified that drives the development of bone marrow failure, treatment is directed toward the underlying disease. In acquired AA, no identifiable genetic cause is identified. The scope of this review will focus on the acquired form of AA.

Table 1 Criteria for severe aplastic anemia[1].
Peripheral blood, CBC findings
Granulocytes< 500/cu mm
Platelets< 20000/cu mm
Reticulocytes< 1%
Bone marrow biopsy findings
Hypoplasia< 25% of normal cellularity
25%-50% of normal cellularity with < 30% hematopoietic cells

Acquired AA can be triggered by exposure to viruses, medications, or noxious chemicals but, for most patients, no inciting event is usually pinpointed. The onset of AA tends to occur in young adults or in elderly patients[2]. The incidence of AA is higher in Asian populations, affecting 3.9-7 patients per million, compared to European populations where 2-2.4 patients per million are affected[2]. Males and females are affected equally[2].

Once a patient is diagnosed with AA, supportive care is initiated and frequent blood and platelet transfusions are performed. Standard-of-care treatment is based on whether the patient has a human leukocyte antigen (HLA)-matched related donor. If a matched donor is available, then definitive treatment with hematopoietic cell transplantation (HCT) is recommended. Patients that undergo matched related donor HCT generally have good outcomes with overall survival approaching 90%[3]. In patients without an HLA-matched donor, accounting for approximately 70% of patients, unrelated or alternative donor transplants have generally been avoided as first-line therapy given the risk of morbidity and mortality associated with transplantation. These patients are treated with a course of immunosuppression with equine anti-thymocyte globulin (ATG) and cyclosporine A (CSA).

A majority of patients without a matched related donor show an initial response to immunosuppression[3]. However, approximately 30% of AA patients do not respond to immunosuppression or have recurrence of cytopenias with weaning immunosuppression[3-5]. For these patients, second-line therapies such as Cyclophosphamide or Eltrombopag or alternative HCT is pursued, using either cord blood, unrelated or haploidentical related donors. An increasing number of AA patients are requiring alternative donor HCT; their outcomes have continued to improve with an overall survival of 80%-90%[6,7]. In addition, recent studies have shown similar outcomes with upfront matched-unrelated donor HCT and matched-sibling donor HCT, further underscoring the role of HCT in treating AA[8].


Although our understanding of the pathogenesis of AA is increasing, it remains incomplete thereby limiting the development and implementation of targeted treatment options for these patients.

Immune-mediated stem cell destruction and impaired hematopoiesis

The observation that many AA patients show clinical improvement in blood counts after treatment with immunosuppression points towards an immune-mediated etiology for the disorder. For example, there is growing evidence that there is increased T-cell activation in patients with AA[3,4,9-11]. Many scientists are working to identify possible inciting factors triggering aberrant T-cell activation in idiopathic AA patients but the primary cause has not yet been fully elucidated. What is known is that effector memory T-cells, which are known to play a role in autoimmunity, are increased in patients with AA[9,12]. In addition, CD8+ T-cells are expanded in AA patients and they show restricted T-cell receptor (TCR) expression[13]. Some studies suggest that the TCRs themselves show increased expression of CD3-zeta and co-stimulatory molecule CD28 promoting T-cell activation[14], whereas other studies suggest a restricted TCR with decreased CD3-zeta expression but with aberrant activity[15].

AA patients also show a shift to a predominantly pro-inflammatory Th1 T-cell phenotype[10,16]; this appears to be at least partly triggered by increased expression of the transcription factor T-bet[10,11]. These Th1 T-cells, in turn, increase production of interferon-γ (INF-γ)[10,16]. INF-γ has been shown to impair long-term colony formation by hematopoietic progenitor cells in vitro suggesting impaired hematopoietic differentiation potential[16]. INF-γ also induces HSCs (CD34+ cells) to undergo apoptosis[9]. In addition to the increased T-cell activation, T-regulatory cells, which have suppressor functions, are decreased in AA patients[17,18]. By this proposed mechanism, the INF-γ producing Th1 cells deplete the marrow of HSCs, leading to the clinically-apparent pancytopenia and bone marrow hypoplasia that is observed.

Impaired MSC function

MSCs are found in adipose tissue, umbilical cords, and the bone marrow. MSCs have the ability to differentiate into other cell types such as chondrocytes, adipocytes, and osteoblasts, and can self-proliferate, maintaining a phenotype of “stemness”[19]. Bone marrow-derived MSCs lie within the stroma of the marrow and play crucial roles in immunomodulation and hematopoietic support.

Normal MSC function has been shown to include interactions with various immune cells including T-cells, B-cells, NK cells, and monocytes in in vitro studies[20-24]. In culture, MSCs inhibit proliferation of activated T-cells (both CD4+ and CD8+ cells) by halting cell cycle progression through the G0/G1 phase[20-24]. Although T-cells can be appropriately activated, they enter a state of senescence in the presence of MSCs[21,22]. This immunomodulatory function relies primarily on secreted factors but is also enhanced by cell-cell contact[21,22,25,26]. IFN-γ has been strongly implicated in this phenomenon as well as indoleamine 2,3-dioxygenase (IDO), hepatocyte growth factor, transforming growth factor β (TGFβ), HLA-G5, IL-10, and PGE2[20-23,27]. In the presence of allostimulated T-cells, MSCs stimulate differentiation of T-cells into T-regulatory cells, which appears to be mediated by HLA-G[27]. However, others have challenged this finding[23]. In addition to inhibition of T-cell proliferation, MSCs similarly inhibit proliferation of resting NK-cells[23,26] and B-cells[25]. Monocytes in the presence of MSCs change their phenotype and arrest in G0; they are unable to differentiate into antigen presenting cells (APCs)[28,29]. Further on this, MSCs themselves have the potential to act as APCs. At baseline, MSCs have low levels of MHC class I and II expression but this is altered by IFN-γ. In the presence of IFN-γ MHC class I is upregulated, protecting MSCs from NK-mediated cell lysis[26]. Although at low levels of IFN-γ MHC class II is present, higher concentration of this potent immunomodulatory cytokine lead to downregulation of MHC-II and prevent MSCs from acting as APCs[30,31].

MSCs are also instrumental in supporting hematopoiesis. Recent in vitro 3-D models of the hematopoietic niche have been generated using a bio-derived bone scaffold, MSCs, and osteoblasts, which can independently produce extracellular matrix and secrete cytokines that stimulate proliferation of hematopoietic progenitor cells (HPCs)[32]. MSCs create a scaffold for HPCs by upregulating adhesion molecules such as integrin subunit beta (ITGB1) and enhance HPC proliferation via upregulation of Twist-1 and CXCL12[33,34].

The above notwithstanding, data on MSC function in patients with AA has been conflicting. Some studies have identified distinctly abnormal MSCs from patients with AA[35-41]. Gene expression profiling identified over 300 genes that were differentially expressed in MSCs from AA patients compared with healthy controls[39]. This included upregulation of genes involved in apoptosis, adipogenesis, and the immune response[39]. Kastrinaki et al[37] reported increased MSC apoptosis in AA patients. Further, MSCs from AA patients have reduced proliferation potential[35,38,39], mediated by decreased CXCL12 and FGF1 expression[36,42]. In addition, a number of studies suggest that MSCs from AA patients show defective differentiation with an increased preponderance to form adipocytes[37,41]. Patients with AA have decreased GATA2 expression and increased PPARγ expression in their MSCs, in turn leading to increased adipocyte differentiation[40]. This has been supported by findings in a mouse model of immune-mediated AA, where inhibition of PPARγ improves bone marrow cellularity and suppresses T-cell activation and proliferation[43].

Despite these interesting findings, some other groups have found opposite results - mainly that MSCs maintain their immunomodulatory properties in patients with AA[44-46]. Indeed, MSCs from AA patients have been shown by some labs to have similar morphology and differentiation potential and inhibit T-cell proliferation similar to control MSCs[44-46]. The discrepancy between these studies and the ones described above may be related to different patient populations (including limited patient numbers), evaluation at different times during treatment, different culture techniques, and differential analyses performed.

Although the in vitro experimental data may be somewhat conflicting, MSCs remain an attractive target for treatment of AA, rooted in their role in the pathophysiology of this disorder. The known function of MSCs and the effect of their dysfunction can connect many observations in AA. For example, when MSC function is impaired, HPCs cannot adequately proliferate, activated T-cells are not suppressed, and the bone marrow architecture changes. We hypothesize that this may correlate with impaired hematopoiesis and pancytopenia, destruction of HSCs by activated T-cells, and increased adipocyte differentiation in a hypoplastic bone marrow - all findings seen in AA patients.


MSCs have been utilized in the settings of therapy for other disorders due to their immunomodulatory and proliferative functions. Most attention has been focused on MSCs for the treatment of refractory gastrointestinal graft-vs-host disease (GvHD). MSCs have been shown to be effective in treating both adults and children with steroid-refractory acute gastrointestinal GvHD - with response rates of over 50%[47,48]. The mechanism for MSC improvement in this disease is thought to be related to immune suppression of allo-reactive T-cells[48]. There is also the possibility that the MSCs may be aiding in tissue regeneration and healing. Similar to the work in GvHD, MSCs have produced improvements in treatment of refractory inflammatory bowel disease and multiple sclerosis, again likely harnessing their immunosuppressive properties[49-52]. MSCs have also shown promise in neurologic diseases - repair in spinal cord injuries, stroke and amyotrophic lateral sclerosis - and in cardiac regeneration after infarction or cardiomyopathy[53-57].

The early phase studies using MSCs have shown a well-tolerated safety profile. No infusional side effects have been noted. There is a theoretical risk of ectopic tissue or tumor formation given the ability of MSCs to differentiate into multiple cell types. However, few case reports have noted this occurring. In addition, when expanding and culturing MSCs, trypsin is used to collect the cells and trypsin has a risk of mutagenesis. Again, there have been no reports of this adverse effect[58].

MSCs enhance engraftment in HCT for AA

Translation of MSC therapy to AA has been relatively limited. Preliminary studies have attempted to use MSCs as an adjunct to HCT to help enhance engraftment or as primary, monotherapy treatment of AA (Table 2).

Table 2 Summary of the clinical uses of mesenchymal stem cells in aplastic anemia.
TreatmentInterventionGoal (s) of therapyOutcome
MSC as adjunct to HCTMSCs given in conjunction with hematopoietic stem cell transplantationTo prevent graft failure or shorten time to engraftmentImproved donor engraftment
MSC as monotherapyMSCs given aloneFor primary treatment of AAPartial response in some patients

The findings that AA patients may have defective MSCs have introduced the possibility of MSC replacement as a therapeutic modality. In the collective pool of patients that go to HCT, AA patients are at high risk of graft failure. There is evidence that supporting patients with HSCs in addition to MSCs will better support hematopoiesis and engraftment[59-61]. Initial case reports adding MSCs to transplantation were promising. Luan et al[61] reported a case of a patient with severe AA that underwent matched sibling cord blood transplant but had delayed engraftment; after giving a cord-blood-derived MSC infusion, the patient began to engraft and pancytopenia improved. Similarly, a report on 2 patients with severe AA who had graft failure after HCT were given second transplant from the same donor with addition of MSCs from a haploidentical maternal donor and they were able to engraft[59]. MSC infusion has also been used upfront around the time of HSC infusion; this approach shorted engraftment, with neutrophil and platelet engraftment occurring by D12 post-HCT, shorter than historical controls[60,62,63]. In addition, alternative donor transplants including haploidentical donor HCT had shorter engraftment when MSCs were added to the regimen[59,62]. A recent phase II study by Liu et al[64] confirmed these findings when bone marrow-derived MSCs were given with haploidentical HCT, 97.6% of patients had engraftment. These studies have all had small sample sizes but overall reports have not described any significant adverse events and suggest a possible benefit. Similar results were seen with umbilical cord-derived MSC or bone marrow-derived MSCs and with related MSCs and third-party MSCs. Larger randomized trials are needed to further validate these findings[64-66].

MSCs as monotherapy for AA

It is hypothesized that defective MSCs prevent adequate hematopoiesis and infusion of donor MSCs may create an environment more supportive of hematopoiesis. Most studies of MSC infusions as monotherapy have been performed with patients who have been refractory to immunosuppression. One case report described a 68-year-old patient with refractory AA who was unable to proceed to HCT and received 2 haploidentical, bone marrow-derived MSC infusions from her son[67]. Unfortunately the patient died from overwhelming infection, but autopsy showed improved bone marrow stroma but without improvement in hematopoiesis[67]. In another single-arm study, 18 patients were given an infusion of third-party, bone marrow-derived MSCs and 33% of patients showed at least a partial response to treatment, eliminating the need for transfusions[68]. Another single-arm study used weekly infusions of HLA-matched, bone marrow-derived MSCs but found poor MSC bone marrow engraftment[69]. However, of the 9 patients, 3 patients did have a partial response and were able to become transfusion independent[69]. In the largest study to date, 53 patients received bone marrow-derived MSCs from matched, haploidentical, or unrelated donors after in vitro expansion[70]. MSC infusion produced modest responses with an overall response rate in the cohort of 28.4% at 1 year[70]. These preliminary studies support the concept that MSC replacement can improve bone marrow stroma and may alleviate symptoms in some AA patients. However, larger studies are needed to evaluate the utility of MSCs further.


As we learn more about the biology of AA, the biology of MSCs, the biology of the bone marrow microenvironment, and as we learn how to safely grow and manipulate human cells, we are moving into an exciting phase of personalized biologic therapy for bone marrow failure.

To date, most of the studies referenced in this review point to the promise of MSC therapy in this context. However, these studies have not been sufficiently powered to fully help us understand the role these therapies play in the treatment of AA. As marrow failure is a rare disease, future studies will require novel study design and outcome measures to help the field advance properly. Therefore, basic scientists, cell therapists, and statisticians will be required to join clinicians in developing translational clinical trials that are able to “molecule by molecule”, “pathway by pathway”, “protein by protein” solve the Rubik’s Cube of an individual’s bone marrow failure and translate that puzzle solving into safe and effective care.

The treatment options are limitless, which is both daunting and exciting. We envision that a patient’s biology will determine what treatments they will be offered. Instead of devising treatments for a heterogeneous disease process, we envision that the genomics and proteomics revolution will lead to an improved understanding of the patient’s individual biology - which will then translate into a rational MSC-based treatment. With such a rare disease as AA, this will require extensive data sharing and evaluation, around the globe, in order to realize the dream of personalized biologic therapy for bone marrow syndromes. Recent breakthroughs in the clinical implementation of gene therapy also offer the possibility of precise modulation of the niche to directly address the unique needs of each patient.


Although our understanding of the etiology of AA is increasing, there remains limited development of targeted treatment options. MSCs, which modulate immune response and help enhance proliferation of HSCs, may be an attractive treatment option. Limited studies have shown modest improvement in AA when given as monotherapy and seem to help enhance engraftment when given in combination with HCT. Further clinical research and basic science studies need to be performed in this area.


Manuscript source: Unsolicited manuscript

Specialty type: Cell and tissue engineering

Country of origin: United States

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P- Reviewer: Cui W, Goebel WS, Kiselev SL, Pixley JS, Ramírez M, Wakao H S- Editor: Ji FF L- Editor: A E- Editor: Lu YJ

1.  Camitta BM, Thomas ED, Nathan DG, Santos G, Gordon-Smith EC, Gale RP, Rappeport JM, Storb R. Severe aplastic anemia: a prospective study of the effect of early marrow transplantation on acute mortality. Blood. 1976;48:63-70.  [PubMed]  [DOI]  [Cited in This Article: ]
2.  Young NS, Kaufman DW. The epidemiology of acquired aplastic anemia. Haematologica. 2008;93:489-492.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 116]  [Cited by in F6Publishing: 117]  [Article Influence: 7.3]  [Reference Citation Analysis (0)]
3.  Young NS. Acquired aplastic anemia. Ann Intern Med. 2002;136:534-546.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 226]  [Cited by in F6Publishing: 233]  [Article Influence: 10.6]  [Reference Citation Analysis (0)]
4.  Rosenfeld S, Follmann D, Nunez O, Young NS. Antithymocyte globulin and cyclosporine for severe aplastic anemia: association between hematologic response and long-term outcome. JAMA. 2003;289:1130-1135.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 282]  [Cited by in F6Publishing: 298]  [Article Influence: 14.2]  [Reference Citation Analysis (0)]
5.  Frickhofen N, Heimpel H, Kaltwasser JP, Schrezenmeier H; German Aplastic Anemia Study Group. Antithymocyte globulin with or without cyclosporin A: 11-year follow-up of a randomized trial comparing treatments of aplastic anemia. Blood. 2003;101:1236-1242.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 242]  [Cited by in F6Publishing: 261]  [Article Influence: 12.4]  [Reference Citation Analysis (0)]
6.  Bacigalupo A, Sica S. Alternative donor transplants for severe aplastic anemia: current experience. Semin Hematol. 2016;53:115-119.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 17]  [Cited by in F6Publishing: 18]  [Article Influence: 2.3]  [Reference Citation Analysis (0)]
7.  Bacigalupo A. How I treat acquired aplastic anemia. Blood. 2017;129:1428-1436.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 196]  [Cited by in F6Publishing: 231]  [Article Influence: 33.0]  [Reference Citation Analysis (0)]
8.  Dufour C, Veys P, Carraro E, Bhatnagar N, Pillon M, Wynn R, Gibson B, Vora AJ, Steward CG, Ewins AM. Similar outcome of upfront-unrelated and matched sibling stem cell transplantation in idiopathic paediatric aplastic anaemia. A study on behalf of the UK Paediatric BMT Working Party, Paediatric Diseases Working Party and Severe Aplastic Anaemia Working Party of EBMT. Br J Haematol. 2015;171:585-594.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 109]  [Cited by in F6Publishing: 110]  [Article Influence: 12.2]  [Reference Citation Analysis (0)]
9.  Zheng M, Liu C, Fu R, Wang H, Wu Y, Li L, Liu H, Ding S, Shao Z. Abnormal immunomodulatory ability on memory T cells in humans with severe aplastic anemia. Int J Clin Exp Pathol. 2015;8:3659-3669.  [PubMed]  [DOI]  [Cited in This Article: ]
10.  Du HZ, Wang Q, Ji J, Shen BM, Wei SC, Liu LJ, Ding J, Ma DX, Wang W, Peng J. Expression of IL-27, Th1 and Th17 in patients with aplastic anemia. J Clin Immunol. 2013;33:436-445.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 17]  [Cited by in F6Publishing: 17]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
11.  Solomou EE, Keyvanfar K, Young NS. T-bet, a Th1 transcription factor, is up-regulated in T cells from patients with aplastic anemia. Blood. 2006;107:3983-3991.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 107]  [Cited by in F6Publishing: 114]  [Article Influence: 6.3]  [Reference Citation Analysis (0)]
12.  Hosokawa K, Muranski P, Feng X, Townsley DM, Liu B, Knickelbein J, Keyvanfar K, Dumitriu B, Ito S, Kajigaya S. Memory Stem T Cells in Autoimmune Disease: High Frequency of Circulating CD8+ Memory Stem Cells in Acquired Aplastic Anemia. J Immunol. 2016;196:1568-1578.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 52]  [Cited by in F6Publishing: 62]  [Article Influence: 7.8]  [Reference Citation Analysis (0)]
13.  Chen J, Brandt JS, Ellison FM, Calado RT, Young NS. Defective stromal cell function in a mouse model of infusion-induced bone marrow failure. Exp Hematol. 2005;33:901-908.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 15]  [Article Influence: 0.8]  [Reference Citation Analysis (0)]
14.  Li B, Guo L, Zhang Y, Xiao Y, Wu M, Zhou L, Chen S, Yang L, Lu X, Li Y. Molecular alterations in the TCR signaling pathway in patients with aplastic anemia. J Hematol Oncol. 2016;9:32.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 10]  [Cited by in F6Publishing: 14]  [Article Influence: 1.8]  [Reference Citation Analysis (0)]
15.  Solomou EE, Wong S, Visconte V, Gibellini F, Young NS. Decreased TCR zeta-chain expression in T cells from patients with acquired aplastic anaemia. Br J Haematol. 2007;138:72-76.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 15]  [Cited by in F6Publishing: 16]  [Article Influence: 0.9]  [Reference Citation Analysis (0)]
16.  Smith JN, Kanwar VS, MacNamara KC. Hematopoietic Stem Cell Regulation by Type I and II Interferons in the Pathogenesis of Acquired Aplastic Anemia. Front Immunol. 2016;7:330.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 32]  [Cited by in F6Publishing: 42]  [Article Influence: 5.3]  [Reference Citation Analysis (0)]
17.  Zeng Y, Katsanis E. The complex pathophysiology of acquired aplastic anaemia. Clin Exp Immunol. 2015;180:361-370.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 80]  [Cited by in F6Publishing: 84]  [Article Influence: 9.3]  [Reference Citation Analysis (0)]
18.  Solomou EE, Rezvani K, Mielke S, Malide D, Keyvanfar K, Visconte V, Kajigaya S, Barrett AJ, Young NS. Deficient CD4+ CD25+ FOXP3+ T regulatory cells in acquired aplastic anemia. Blood. 2007;110:1603-1606.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 140]  [Cited by in F6Publishing: 162]  [Article Influence: 9.5]  [Reference Citation Analysis (0)]
19.  Pittenger MF, Mackay AM, Beck SC, Jaiswal RK, Douglas R, Mosca JD, Moorman MA, Simonetti DW, Craig S, Marshak DR. Multilineage potential of adult human mesenchymal stem cells. Science. 1999;284:143-147.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 15372]  [Cited by in F6Publishing: 14736]  [Article Influence: 589.4]  [Reference Citation Analysis (0)]
20.  Cuerquis J, Romieu-Mourez R, François M, Routy JP, Young YK, Zhao J, Eliopoulos N. Human mesenchymal stromal cells transiently increase cytokine production by activated T cells before suppressing T-cell proliferation: effect of interferon-γ and tumor necrosis factor-α stimulation. Cytotherapy. 2014;16:191-202.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 79]  [Cited by in F6Publishing: 86]  [Article Influence: 8.6]  [Reference Citation Analysis (0)]
21.  Di Nicola M, Carlo-Stella C, Magni M, Milanesi M, Longoni PD, Matteucci P, Grisanti S, Gianni AM. Human bone marrow stromal cells suppress T-lymphocyte proliferation induced by cellular or nonspecific mitogenic stimuli. Blood. 2002;99:3838-3843.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2455]  [Cited by in F6Publishing: 2302]  [Article Influence: 104.6]  [Reference Citation Analysis (0)]
22.  Glennie S, Soeiro I, Dyson PJ, Lam EW, Dazzi F. Bone marrow mesenchymal stem cells induce division arrest anergy of activated T cells. Blood. 2005;105:2821-2827.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 825]  [Cited by in F6Publishing: 806]  [Article Influence: 42.4]  [Reference Citation Analysis (0)]
23.  Krampera M, Cosmi L, Angeli R, Pasini A, Liotta F, Andreini A, Santarlasci V, Mazzinghi B, Pizzolo G, Vinante F. Role for interferon-gamma in the immunomodulatory activity of human bone marrow mesenchymal stem cells. Stem Cells. 2006;24:386-398.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 977]  [Cited by in F6Publishing: 982]  [Article Influence: 51.7]  [Reference Citation Analysis (0)]
24.  Bacigalupo A, Valle M, Podestà M, Pitto A, Zocchi E, De Flora A, Pozzi S, Luchetti S, Frassoni F, Van Lint MT. T-cell suppression mediated by mesenchymal stem cells is deficient in patients with severe aplastic anemia. Exp Hematol. 2005;33:819-827.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 88]  [Cited by in F6Publishing: 78]  [Article Influence: 4.1]  [Reference Citation Analysis (0)]
25.  Corcione A, Benvenuto F, Ferretti E, Giunti D, Cappiello V, Cazzanti F, Risso M, Gualandi F, Mancardi GL, Pistoia V. Human mesenchymal stem cells modulate B-cell functions. Blood. 2006;107:367-372.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1263]  [Cited by in F6Publishing: 1235]  [Article Influence: 65.0]  [Reference Citation Analysis (0)]
26.  Spaggiari GM, Capobianco A, Becchetti S, Mingari MC, Moretta L. Mesenchymal stem cell-natural killer cell interactions: evidence that activated NK cells are capable of killing MSCs, whereas MSCs can inhibit IL-2-induced NK-cell proliferation. Blood. 2006;107:1484-1490.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 773]  [Cited by in F6Publishing: 752]  [Article Influence: 39.6]  [Reference Citation Analysis (0)]
27.  Selmani Z, Naji A, Zidi I, Favier B, Gaiffe E, Obert L, Borg C, Saas P, Tiberghien P, Rouas-Freiss N. Human leukocyte antigen-G5 secretion by human mesenchymal stem cells is required to suppress T lymphocyte and natural killer function and to induce CD4+CD25highFOXP3+ regulatory T cells. Stem Cells. 2008;26:212-222.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 762]  [Cited by in F6Publishing: 802]  [Article Influence: 47.2]  [Reference Citation Analysis (0)]
28.  Ramasamy R, Fazekasova H, Lam EW, Soeiro I, Lombardi G, Dazzi F. Mesenchymal stem cells inhibit dendritic cell differentiation and function by preventing entry into the cell cycle. Transplantation. 2007;83:71-76.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 338]  [Cited by in F6Publishing: 323]  [Article Influence: 19.0]  [Reference Citation Analysis (0)]
29.  Cutler AJ, Limbani V, Girdlestone J, Navarrete CV. Umbilical cord-derived mesenchymal stromal cells modulate monocyte function to suppress T cell proliferation. J Immunol. 2010;185:6617-6623.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 130]  [Cited by in F6Publishing: 132]  [Article Influence: 9.4]  [Reference Citation Analysis (0)]
30.  Chan WK, Lau AS, Li JC, Law HK, Lau YL, Chan GC. MHC expression kinetics and immunogenicity of mesenchymal stromal cells after short-term IFN-gamma challenge. Exp Hematol. 2008;36:1545-1555.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 91]  [Cited by in F6Publishing: 80]  [Article Influence: 5.0]  [Reference Citation Analysis (0)]
31.  Chan JL, Tang KC, Patel AP, Bonilla LM, Pierobon N, Ponzio NM, Rameshwar P. Antigen-presenting property of mesenchymal stem cells occurs during a narrow window at low levels of interferon-gamma. Blood. 2006;107:4817-4824.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 305]  [Cited by in F6Publishing: 306]  [Article Influence: 17.0]  [Reference Citation Analysis (0)]
32.  Huang X, Zhu B, Wang X, Xiao R, Wang C. Three-dimensional co-culture of mesenchymal stromal cells and differentiated osteoblasts on human bio-derived bone scaffolds supports active multi-lineage hematopoiesis in vitro: Functional implication of the biomimetic HSC niche. Int J Mol Med. 2016;38:1141-1151.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 35]  [Cited by in F6Publishing: 38]  [Article Influence: 4.8]  [Reference Citation Analysis (0)]
33.  Arthur A, Cakouros D, Cooper L, Nguyen T, Isenmann S, Zannettino AC, Glackin CA, Gronthos S. Twist-1 Enhances Bone Marrow Mesenchymal Stromal Cell Support of Hematopoiesis by Modulating CXCL12 Expression. Stem Cells. 2016;34:504-509.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 14]  [Article Influence: 1.6]  [Reference Citation Analysis (0)]
34.  Wagner W, Roderburg C, Wein F, Diehlmann A, Frankhauser M, Schubert R, Eckstein V, Ho AD. Molecular and secretory profiles of human mesenchymal stromal cells and their abilities to maintain primitive hematopoietic progenitors. Stem Cells. 2007;25:2638-2647.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 172]  [Cited by in F6Publishing: 178]  [Article Influence: 10.5]  [Reference Citation Analysis (0)]
35.  Chao YH, Peng CT, Harn HJ, Chan CK, Wu KH. Poor potential of proliferation and differentiation in bone marrow mesenchymal stem cells derived from children with severe aplastic anemia. Ann Hematol. 2010;89:715-723.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 56]  [Cited by in F6Publishing: 59]  [Article Influence: 4.2]  [Reference Citation Analysis (0)]
36.  Chao YH, Wu KH, Chiou SH, Chiang SF, Huang CY, Yang HC, Chan CK, Peng CT, Wu HP, Chow KC. Downregulated CXCL12 expression in mesenchymal stem cells associated with severe aplastic anemia in children. Ann Hematol. 2015;94:13-22.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 14]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
37.  Kastrinaki MC, Pavlaki K, Batsali AK, Kouvidi E, Mavroudi I, Pontikoglou C, Papadaki HA. Mesenchymal stem cells in immune-mediated bone marrow failure syndromes. Clin Dev Immunol. 2013;2013:265608.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 20]  [Cited by in F6Publishing: 20]  [Article Influence: 1.8]  [Reference Citation Analysis (0)]
38.  Hamzic E, Whiting K, Gordon Smith E, Pettengell R. Characterization of bone marrow mesenchymal stromal cells in aplastic anaemia. Br J Haematol. 2015;169:804-813.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 36]  [Cited by in F6Publishing: 38]  [Article Influence: 4.2]  [Reference Citation Analysis (0)]
39.  Li J, Yang S, Lu S, Zhao H, Feng J, Li W, Ma F, Ren Q, Liu B, Zhang L. Differential gene expression profile associated with the abnormality of bone marrow mesenchymal stem cells in aplastic anemia. PLoS One. 2012;7:e47764.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 40]  [Cited by in F6Publishing: 47]  [Article Influence: 3.9]  [Reference Citation Analysis (0)]
40.  Xu Y, Takahashi Y, Wang Y, Hama A, Nishio N, Muramatsu H, Tanaka M, Yoshida N, Villalobos IB, Yagasaki H. Downregulation of GATA-2 and overexpression of adipogenic gene-PPARgamma in mesenchymal stem cells from patients with aplastic anemia. Exp Hematol. 2009;37:1393-1399.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 36]  [Cited by in F6Publishing: 34]  [Article Influence: 2.3]  [Reference Citation Analysis (0)]
41.  Tripathy NK, Singh SP, Nityanand S. Enhanced adipogenicity of bone marrow mesenchymal stem cells in aplastic anemia. Stem Cells Int. 2014;2014:276862.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 16]  [Cited by in F6Publishing: 17]  [Article Influence: 1.7]  [Reference Citation Analysis (0)]
42.  Jiang S, Xia M, Yang J, Shao J, Liao X, Zhu J, Jiang H. Novel insights into a treatment for aplastic anemia based on the advanced proliferation of bone marrowderived mesenchymal stem cells induced by fibroblast growth factor 1. Mol Med Rep. 2015;12:7877-7882.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 15]  [Article Influence: 1.7]  [Reference Citation Analysis (0)]
43.  Sato K, Feng X, Chen J, Li J, Muranski P, Desierto MJ, Keyvanfar K, Malide D, Kajigaya S, Young NS. PPARγ antagonist attenuates mouse immune-mediated bone marrow failure by inhibition of T cell function. Haematologica. 2016;101:57-67.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 12]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
44.  Bueno C, Roldan M, Anguita E, Romero-Moya D, Martín-Antonio B, Rosu-Myles M, del Cañizo C, Campos F, García R, Gómez-Casares M. Bone marrow mesenchymal stem cells from patients with aplastic anemia maintain functional and immune properties and do not contribute to the pathogenesis of the disease. Haematologica. 2014;99:1168-1175.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 28]  [Cited by in F6Publishing: 31]  [Article Influence: 3.1]  [Reference Citation Analysis (0)]
45.  Xu Y, Takahashi Y, Yoshimi A, Tanaka M, Yagasaki H, Kojima S. Immunosuppressive activity of mesenchymal stem cells is not decreased in children with aplastic anemia. Int J Hematol. 2009;89:126-127.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 7]  [Cited by in F6Publishing: 7]  [Article Influence: 0.5]  [Reference Citation Analysis (0)]
46.  Michelozzi IM, Pievani A, Pagni F, Antolini L, Verna M, Corti P, Rovelli A, Riminucci M, Dazzi F, Biondi A. Human aplastic anaemia-derived mesenchymal stromal cells form functional haematopoietic stem cell niche in vivo. Br J Haematol. 2016;.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 12]  [Article Influence: 1.5]  [Reference Citation Analysis (0)]
47.  Kurtzberg J, Prockop S, Teira P, Bittencourt H, Lewis V, Chan KW, Horn B, Yu L, Talano JA, Nemecek E. Allogeneic human mesenchymal stem cell therapy (remestemcel-L, Prochymal) as a rescue agent for severe refractory acute graft-versus-host disease in pediatric patients. Biol Blood Marrow Transplant. 2014;20:229-235.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 165]  [Cited by in F6Publishing: 158]  [Article Influence: 14.4]  [Reference Citation Analysis (0)]
48.  Le Blanc K, Frassoni F, Ball L, Locatelli F, Roelofs H, Lewis I, Lanino E, Sundberg B, Bernardo ME, Remberger M. Mesenchymal stem cells for treatment of steroid-resistant, severe, acute graft-versus-host disease: a phase II study. Lancet. 2008;371:1579-1586.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2047]  [Cited by in F6Publishing: 1966]  [Article Influence: 122.9]  [Reference Citation Analysis (0)]
49.  Duijvestein M, van den Brink GR, Hommes DW. Stem cells as potential novel therapeutic strategy for inflammatory bowel disease. J Crohns Colitis. 2008;2:99-106.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 20]  [Cited by in F6Publishing: 20]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
50.  Llufriu S, Sepúlveda M, Blanco Y, Marín P, Moreno B, Berenguer J, Gabilondo I, Martínez-Heras E, Sola-Valls N, Arnaiz JA. Randomized placebo-controlled phase II trial of autologous mesenchymal stem cells in multiple sclerosis. PLoS One. 2014;9:e113936.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 108]  [Cited by in F6Publishing: 111]  [Article Influence: 11.1]  [Reference Citation Analysis (0)]
51.  Meamar R, Nematollahi S, Dehghani L, Mirmosayyeb O, Shayegannejad V, Basiri K, Tanhaei AP. The role of stem cell therapy in multiple sclerosis: An overview of the current status of the clinical studies. Adv Biomed Res. 2016;5:46.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 21]  [Cited by in F6Publishing: 25]  [Article Influence: 3.1]  [Reference Citation Analysis (0)]
52.  Forbes GM, Sturm MJ, Leong RW, Sparrow MP, Segarajasingam D, Cummins AG, Phillips M, Herrmann RP. A phase 2 study of allogeneic mesenchymal stromal cells for luminal Crohn’s disease refractory to biologic therapy. Clin Gastroenterol Hepatol. 2014;12:64-71.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 253]  [Cited by in F6Publishing: 238]  [Article Influence: 23.8]  [Reference Citation Analysis (0)]
53.  Mendonça MV, Larocca TF, de Freitas Souza BS, Villarreal CF, Silva LF, Matos AC, Novaes MA, Bahia CM, de Oliveira Melo Martinez AC, Kaneto CM. Safety and neurological assessments after autologous transplantation of bone marrow mesenchymal stem cells in subjects with chronic spinal cord injury. Stem Cell Res Ther. 2014;5:126.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 129]  [Cited by in F6Publishing: 131]  [Article Influence: 13.1]  [Reference Citation Analysis (0)]
54.  Díez-Tejedor E, Gutiérrez-Fernández M, Martínez-Sánchez P, Rodríguez-Frutos B, Ruiz-Ares G, Lara ML, Gimeno BF. Reparative therapy for acute ischemic stroke with allogeneic mesenchymal stem cells from adipose tissue: a safety assessment: a phase II randomized, double-blind, placebo-controlled, single-center, pilot clinical trial. J Stroke Cerebrovasc Dis. 2014;23:2694-2700.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 98]  [Cited by in F6Publishing: 104]  [Article Influence: 10.4]  [Reference Citation Analysis (0)]
55.  Mazzini L, Ferrero I, Luparello V, Rustichelli D, Gunetti M, Mareschi K, Testa L, Stecco A, Tarletti R, Miglioretti M. Mesenchymal stem cell transplantation in amyotrophic lateral sclerosis: A Phase I clinical trial. Exp Neurol. 2010;223:229-237.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 278]  [Cited by in F6Publishing: 294]  [Article Influence: 19.6]  [Reference Citation Analysis (0)]
56.  Can A, Ulus AT, Cinar O, Topal Celikkan F, Simsek E, Akyol M, Canpolat U, Erturk M, Kara F, Ilhan O. Human Umbilical Cord Mesenchymal Stromal Cell Transplantation in Myocardial Ischemia (HUC-HEART Trial). A Study Protocol of a Phase 1/2, Controlled and Randomized Trial in Combination with Coronary Artery Bypass Grafting. Stem Cell Rev. 2015;11:752-760.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 28]  [Cited by in F6Publishing: 24]  [Article Influence: 3.0]  [Reference Citation Analysis (0)]
57.  Mushtaq M, DiFede DL, Golpanian S, Khan A, Gomes SA, Mendizabal A, Heldman AW, Hare JM. Rationale and design of the Percutaneous Stem Cell Injection Delivery Effects on Neomyogenesis in Dilated Cardiomyopathy (the POSEIDON-DCM study): a phase I/II, randomized pilot study of the comparative safety and efficacy of transendocardial injection of autologous mesenchymal stem cell vs. allogeneic mesenchymal stem cells in patients with non-ischemic dilated cardiomyopathy. J Cardiovasc Transl Res. 2014;7:769-780.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 35]  [Cited by in F6Publishing: 27]  [Article Influence: 2.7]  [Reference Citation Analysis (0)]
58.  Habib HS, Halawa TF, Atta HM. Therapeutic applications of mesenchymal stroma cells in pediatric diseases: current aspects and future perspectives. Med Sci Monit. 2011;17:RA233-RA239.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 8]  [Article Influence: 0.7]  [Reference Citation Analysis (0)]
59.  Fang B, Li N, Song Y, Li J, Zhao RC, Ma Y. Cotransplantation of haploidentical mesenchymal stem cells to enhance engraftment of hematopoietic stem cells and to reduce the risk of graft failure in two children with severe aplastic anemia. Pediatr Transplant. 2009;13:499-502.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 42]  [Cited by in F6Publishing: 45]  [Article Influence: 3.0]  [Reference Citation Analysis (0)]
60.  Le Blanc K, Samuelsson H, Gustafsson B, Remberger M, Sundberg B, Arvidson J, Ljungman P, Lönnies H, Nava S, Ringdén O. Transplantation of mesenchymal stem cells to enhance engraftment of hematopoietic stem cells. Leukemia. 2007;21:1733-1738.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 338]  [Cited by in F6Publishing: 310]  [Article Influence: 18.2]  [Reference Citation Analysis (0)]
61.  Luan C, Chen R, Chen B, Ding J, Ni M. Umbilical cord blood transplantation supplemented with the infusion of mesenchymal stem cell for an adolescent patient with severe aplastic anemia: a case report and review of literature. Patient Prefer Adherence. 2015;9:759-765.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 3]  [Article Influence: 0.3]  [Reference Citation Analysis (0)]
62.  Wang H, Yan H, Wang Z, Zhu L, Liu J, Guo Z. Cotransplantation of allogeneic mesenchymal and hematopoietic stem cells in children with aplastic anemia. Pediatrics. 2012;129:e1612-e1615.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 27]  [Cited by in F6Publishing: 27]  [Article Influence: 2.3]  [Reference Citation Analysis (0)]
63.  Li XH, Gao CJ, Da WM, Cao YB, Wang ZH, Xu LX, Wu YM, Liu B, Liu ZY, Yan B. Reduced intensity conditioning, combined transplantation of haploidentical hematopoietic stem cells and mesenchymal stem cells in patients with severe aplastic anemia. PLoS One. 2014;9:e89666.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 36]  [Cited by in F6Publishing: 39]  [Article Influence: 3.9]  [Reference Citation Analysis (0)]
64.  Liu Z, Zhang Y, Xiao H, Yao Z, Zhang H, Liu Q, Wu B, Nie D, Li Y, Pang Y. Cotransplantation of bone marrow-derived mesenchymal stem cells in haploidentical hematopoietic stem cell transplantation in patients with severe aplastic anemia: an interim summary for a multicenter phase II trial results. Bone Marrow Transplant. 2017;52:1080.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 29]  [Cited by in F6Publishing: 32]  [Article Influence: 4.6]  [Reference Citation Analysis (0)]
65.  Chao YH, Tsai C, Peng CT, Wu HP, Chan CK, Weng T, Wu KH. Cotransplantation of umbilical cord MSCs to enhance engraftment of hematopoietic stem cells in patients with severe aplastic anemia. Bone Marrow Transplant. 2011;46:1391-1392.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 31]  [Cited by in F6Publishing: 33]  [Article Influence: 2.4]  [Reference Citation Analysis (0)]
66.  Wu Y, Cao Y, Li X, Xu L, Wang Z, Liu P, Yan P, Liu Z, Wang J, Jiang S. Cotransplantation of haploidentical hematopoietic and umbilical cord mesenchymal stem cells for severe aplastic anemia: successful engraftment and mild GVHD. Stem Cell Res. 2014;12:132-138.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 76]  [Cited by in F6Publishing: 72]  [Article Influence: 6.5]  [Reference Citation Analysis (0)]
67.  Fouillard L, Bensidhoum M, Bories D, Bonte H, Lopez M, Moseley AM, Smith A, Lesage S, Beaujean F, Thierry D. Engraftment of allogeneic mesenchymal stem cells in the bone marrow of a patient with severe idiopathic aplastic anemia improves stroma. Leukemia. 2003;17:474-476.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 134]  [Cited by in F6Publishing: 137]  [Article Influence: 6.5]  [Reference Citation Analysis (0)]
68.  Xiao Y, Jiang ZJ, Pang Y, Li L, Gao Y, Xiao HW, Li YH, Zhang H, Liu Q. Efficacy and safety of mesenchymal stromal cell treatment from related donors for patients with refractory aplastic anemia. Cytotherapy. 2013;15:760-766.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 31]  [Cited by in F6Publishing: 36]  [Article Influence: 3.3]  [Reference Citation Analysis (0)]
69.  Clé DV, Santana-Lemos B, Tellechea MF, Prata KL, Orellana MD, Covas DT, Calado RT. Intravenous infusion of allogeneic mesenchymal stromal cells in refractory or relapsed aplastic anemia. Cytotherapy. 2015;17:1696-1705.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 20]  [Cited by in F6Publishing: 22]  [Article Influence: 2.8]  [Reference Citation Analysis (0)]
70.  Pang Y, Xiao HW, Zhang H, Liu ZH, Li L, Gao Y, Li HB, Jiang ZJ, Tan H, Lin JR. Allogeneic Bone Marrow-Derived Mesenchymal Stromal Cells Expanded In Vitro for Treatment of Aplastic Anemia: A Multicenter Phase II Trial. Stem Cells Transl Med. 2017;6:1569-1575.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 13]  [Cited by in F6Publishing: 14]  [Article Influence: 2.0]  [Reference Citation Analysis (0)]