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Blood, 15 March 2005, Vol. 105, No. 6, pp. 2585-2593. Prepublished online as a Blood First Edition Paper on October 7, 2004; DOI 10.1182/blood-2002-11-3463. This Article Full Text (PDF) All Versions of this Article: 2002-11-3463v1 105/6/2585    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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Gur, H. Articles by Reisner, Y. Search for Related Content PubMed PubMed Citation Articles by Gur, H. Articles by Reisner, Y. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 12, 2002 Accepted October 4, 2004 Immune regulatory activity of CD34+ progenitor cells: evidence for a deletion based mechanism mediated by TNF- Hilit Gur, Rita Krauthgamer, Esther Bachar-Lustig, Helena Katchman, Rinat Arbel-Goren, Alain Berrebi, Tirza Klein, Arnon Nagler, Antonio Tabilio, Massimo F Martelli, and Yair Reisner* Department of Immunology, Weizmann Institute of Science, Rehovot, Israel Department of Hematology, Kaplan Medical Center, Rehovot, Israel Department of Tissue Typing, Rabin Medical Center, Petah Tikva, Israel Department of Bone Marrow Transplantation, Sheba Medical Center, Tel Hashomer, Israel Department of Hematology, University of Perugia, Perugia, Italy * Corresponding author; email: yair.reisner{at}weizmann.ac.il. Abstract Previous studies suggest that cells within the CD34+ hematopoietic stem cell compartment are endowed with immune regulatory activity. Furthermore, it is possible to expand the human regulatory cells upon short-term culture of purified CD34+ cells with an early-acting cytokine cocktail. We now show that addition of anti-CD28, anti-CD2, IL-2, anti-IL-10, or IL-12 to the bulk MLR cannot reverse the inhibitory activity of the CD34+ cells, rulling out anergy based mechanisms, or mechanisms involving Th1-Th2 skewing. Furthermore, phenotyping of cells present after addition of CD34+ cells to the bulk MLR, ruled out potential induction of plasmacytoid dendritic precursors, known to be endowed with regulatory activity. In contrast, the inhibitory activity of CD34+ cells could be reversed by adding the caspase inhibitor BD-FMK to the bulk MLR, indicating a deletion based mechanism. The deletion can be inhibited by anti-TNF- and not by anti-TGF-, suggesting a potential role for TNF-a in the regulatory activity of CD34+ cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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