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Blood, 15 September 2007, Vol. 110, No. 6, pp. 2197-2200. Prepublished online as a Blood First Edition Paper on May 23, 2007; DOI 10.1182/blood-2007-04-083162. This Article Full Text (PDF) All Versions of this Article: blood-2007-04-083162v1 110/6/2197    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Gieseke, F. Articles by Muller, I. Search for Related Content PubMed PubMed Citation Articles by Gieseke, F. Articles by Muller, I. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted April 2, 2007 Accepted May 4, 2007 Human multipotent mesenchymal stromal cells inhibit proliferation of PBMC independently of IFNR1-signaling and IDO expression Friederike Gieseke, Burkhardt Schutt, Susanne Viebahn, Ewa Koscielniak, Wilhelm Friedrich, Rupert Handgretinger, and Ingo Muller* Dept of General Pediatrics, Hematology, and Oncology, University Children's Hospital, Tuebingen, Germany Division of Pediatric Endocrinology, Univeristy Children's Hospital, Tuebingen, Germany Olga-Hospital, Stuttgart, Germany University Children's Hospital, Ulm, Germany * Corresponding author; email: ingo.mueller{at}med.uni-tuebingen.de. Multipotent mesenchymal stromal cells (MSC) inhibit proliferation, helper and effector functions in most if not all PBMC subpopulations in vitro. The molecular mechanism is widely thought to imply tryptophan degradation by the IFN-induced expression of indoleamine 2,3-dioxygenase (IDO). However, IDO inhibitors were not able to restore proliferation of PBMC in each case. Moreover, human MSC with an IFN-R1 defect inhibited proliferation of HLA-mismatched PBMC to a similar extent as control MSC. In contrast to healthy MSC, IFNR1-deficient MSC showed no detectable mRNA for IDO - neither in the absence nor in the presence of recombinant human IFN, nor in co-culture with HLA-mismatched PBMC. Based on gene expression profiling we were able to show that insulin-like growth factor binding proteins contribute to the inhibitory mechanism of MSC. Taken together, human MSC exert important immunomodulatory functions in the absence of IFN-R1 signaling and IDO, partially accounted for by IGF-binding proteins. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. Ding, D. Xu, G. Feng, A. Bushell, R. J. Muschel, and K. J. Wood Mesenchymal Stem Cells Prevent the Rejection of Fully Allogenic Islet Grafts by the Immunosuppressive Activity of Matrix Metalloproteinase-2 and -9 Diabetes, August 1, 2009; 58(8): 1797 - 1806. [Abstract] [Full Text] [PDF] M. A. Haniffa, M. P. Collin, C. D. Buckley, and F. Dazzi Mesenchymal stem cells: the fibroblasts' new clothes? Haematologica, February 1, 2009; 94(2): 258 - 263. [Abstract] [Full Text] [PDF] A. W Lee, H. Grifka, and S. Yu Gab2 Is a Key Determinant of Mononuclear Phagocyte Development and a Regulator of Macrophage Recruitment in Acute Inflammation Blood (ASH Annual Meeting Abstracts), November 16, 2008; 112(11): 3857 - 3857. [Abstract]

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