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Ann Thorac Surg 2003;76:339-340
© 2003 The Society of Thoracic Surgeons
a Department of Cardiothoracic and Vascular Surgery, National University of Singapore, Singapore 117597, Singapore
b 10-Medical DriveNational University of Singapore, Singapore-117597, Singapore
c 1770 Moriah Woods BlvdSuite 18Cell Therapy, Inc, Memphis, TN 38117-7126 USA
d Department of Cardiac, Thoracic and Vascular Surgery, National University Hospital, 5 Lower Kent Ridge Rd, Singapore 119074, Singapore
e-mail: khhaider{at}hotmail.com
e-mail: sursinkw{at}nus.edu.sg
To the Editor:
Saito and colleagues [1] wrote an interesting report that challenges the concept of immune tolerance. They injected mice bone marrow stromal cells (BMSCs) into immunocompetent rats and demonstrated engraftment and survival. The results reveal the immune privileged nature of the BMSCs. It is well known that organ and cell transplantation between different individuals of the same species is poorly tolerated without immunosuppression. Xenotransplantation is even more problematic because of rapid rejection. This recent report of successful xenotransplantation of BMSCs into immunocompetent recipients is perplexing.
In our studies of human myoblasts labeled with lac-z reporter gene [unpublished data], we found that the cells could be transplanted into the ischemic heart of pigs with transient immunosuppression. Cyclosporine (5 mg · kg-1 · d-1) given for 6 weeks after cell transplantation allowed successful engraftment of the myoblasts in the porcine heart with robust expression of lac-z for up to 30 weeks of observation in host tissue even after the discontinuation of immunosuppression.
The study by Saito and colleagues [1] shows that the histocompatibility barriers have "weaker links" that can be crossed without immunosuppression. This is important and needs further exploration. The authors based their observation solely on the expression of x-gal staining, which would have been more conclusive with evidence of the absence of immune cell infiltration at the site of the graft. Moreover, the authors failed to provide quantitative assessment of donor cells migrating to the myocardium. Quantification of donor cells reaching the injured myocardium and their transformation into cardiomyocytes might have imparted relevance to this study in the clinical perspective. On the basis of the figures in the study [1], the number of cells reaching the myocardium is too insignificant to impart functional improvement to host myocardium. Further, we believe that quantification of the migrating donor cells might also provide a clue regarding the efficiency of the host’s own bone marrow cells to migrate and supplement the ability of the myocardium to regenerate. Consistent with previously published data [2] the study provides impetus to the belief that in the event of myocardial injury, bone marrow stem cells undergo differentiation to initiate and perform the repair process.
In the light of this report [1] and other recent studies, the current understanding of immune tolerance needs to be reviewed more carefully.
References
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