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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.
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TRANSPLANTATION
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
From the 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; and Department of Hematology, University of Perugia, Italy.
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, interleukin-2 (IL-2), anti–IL-10, or IL-12 to the bulk mixed lymphocyte reaction (MLR) cannot reverse the inhibitory activity of the CD34+ cells, ruling 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–tumor necrosis factor- (anti–TNF-) and not by anti–transforming growth factor- (anti–TGF-), suggesting a potential role for TNF- in the regulatory activity of CD34+ cells.
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