Sensitivity of myeloid progenitors to NK‐cell depletion

Fardoun‐Joalland, D.; Texeira-Lebrun, G; Jouan-Beades, F; Lenormand, Bernard; Dzondo‐Gadet, M.; Jp, Vannier

doi:10.1002/ajh.2830470408

Cited by 4 publications

(3 citation statements)

References 13 publications

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“…21,22 Yet their actual function has remained controversial, inasmuch as they are potentially capable of exerting both positive and negative effects on hematopoietic progenitor cells through their production of growth-promoting and growth-inhibiting cytokines, such as granulocyte macrophage-colony-stimulating factor and IFN-␥, respectively. 23 NK cells are potent cytotoxic effectors that co-express several ligands of the TNF death receptor family, such as FasL, TNF-␣, or TRAIL.…”

Section: Discussionmentioning

confidence: 99%

Natural killer cell–dependent apoptosis of peripheral murine hematopoietic progenitor cells in response to Fas cross-linking: involvement of tumor necrosis factor-α

Moreau

Leite‐de‐Moraes

Ezine

et al. 2001

Blood

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Recently, a marked extramedullary myelopoiesis in Fas/CD95-or FasL/CD95L-deficient mice has been reported. In the present in vitro study, the mechanisms underlying Fas-induced apoptosis of normal peripheral colony-forming unit-C (CFU-C) progenitors in the spleen were analyzed. Surprisingly, it was found that clonogenic progenitors were protected from ␥IFN plus Fas-induced programmed cell death when Lin ؉ cells were removed from cultured splenocytes. The cells that rendered CFU-C sensitive to the activa-

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Section: Discussionmentioning

confidence: 99%

Natural killer cell–dependent apoptosis of peripheral murine hematopoietic progenitor cells in response to Fas cross-linking: involvement of tumor necrosis factor-α

Moreau

Leite‐de‐Moraes

Ezine

et al. 2001

Blood

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“…Other synergistic hematopoietic growth factors appear to have the ability to up-regulate the receptor expression of other cytokine on hematopoietic progenitors. On another hand, some of our results suggest that IL-12 might act by stimulating accessory cells to secondary cytokine production [20]. The enhancing effect of IL-12 may be mediated indirectly on 5-FU-treated human peripheral CD34 + cells.…”

Section: Human Modelsmentioning

confidence: 71%

IL-12 indirectly enhances proliferation of 5-FU-treated human hematopoietic peripheral blood CD34+ cells

Grafte¹,

Leveque²,

Paysant³

et al. 1998

Am. J. Hematol.

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Interleukin-12 (IL-12) or natural killer cell stimulatory factor (NKSF), has multiple effects on T lymphocytes and natural killer cells. In this study, the effect of IL-12 on human hematopoiesis was studied by analyzing the growth of CD34+ peripheral blood stem cells (PBSC), in steady state. In the presence of Epo, IL-12 alone or in combination with IL-3 or SCF had no effect on the formation of colonies from CD34+ cells. In culture with Epo, G-CSF, and IL-3, the effect of Flt3-ligand (FL) on CD34+ PBSC was investigated in the presence or absence of IL-12. No additional effect of IL-12 was observed when combined with FL. We evaluated 5-FU-treated human CD34+ PBSC proliferation in cultures with Epo, G-CSF, and IL-3, in the presence or absence of IL-12. No cytokine combination enhanced colony formation from 5-FU-treated CD34+ cells. However, in cultures of 5-FU-treated human CD34+ cells, the most efficient combination was IL-3 + Epo + G-CSF + Accessory cells (CD34-). Furthermore, IL-12 enhanced this colony formation significantly. To investigate whether immature CD34+ cells were responsible for FL or SCF, 5-FU-treated human CD34+ cells were cultured with or without IL-12. Whereas no synergistic effect was observed in combination with IL-12, SCF alone significantly enhanced colony formation. However, the colony number was found to be smaller than with the potent combination of accessory cells in the presence of IL-12. These results indicate that accessory cells, lost in CD34+ cell purification, could be partly responsible for an IL-12 effect on immature human PBSC proliferation.

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“…Mature cell populations in fact display lineage-specific functional effects on stem and progenitor cells; platelets ( Foss et al , 2008 ) and NK cells ( Fardoun-Joalland et al , 1994 ) both secrete factors that enhance progenitor expansion, whereas macrophages ( Xu et al , 2000 ) and red blood cells ( Cheshier et al , 2007 ) secrete factors that inhibit progenitor expansion. Stem and progenitor cell fate decisions are regulated by a balance of antagonistic stimulatory versus inhibitory soluble factors ( Cashman et al , 1990 ; Jacobsen et al , 1994 ) produced by distinct cell populations in the microenvironment ( Wright et al , 1979 ).…”

Section: Methodsmentioning

confidence: 99%

Cell–cell interaction networks regulate blood stem and progenitor cell fate

Kirouac

Madlambayan

et al. 2009

Molecular Systems Biology

111

120

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Communication networks between cells and tissues are necessary for homeostasis in multicellular organisms. Intercellular (between cell) communication networks are particularly relevant in stem cell biology, as stem cell fate decisions (self-renewal, proliferation, lineage specification) are tightly regulated based on physiological demand. We have developed a novel mathematical model of blood stem cell development incorporating cell-level kinetic parameters as functions of secreted molecule-mediated intercellular networks. By relation to quantitative cellular assays, our model is capable of predictively simulating many disparate features of both normal and malignant hematopoiesis, relating internal parameters and microenvironmental variables to measurable cell fate outcomes. Through integrated in silico and experimental analyses, we show that blood stem and progenitor cell fate is regulated by cell-cell feedback, and can be controlled non-cell autonomously by dynamically perturbing intercellular signalling. We extend this concept by demonstrating that variability in the secretion rates of the intercellular regulators is sufficient to explain heterogeneity in culture outputs, and that loss of responsiveness to cell-cell feedback signalling is both necessary and sufficient to induce leukemic transformation in silico.

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Sensitivity of myeloid progenitors to NK‐cell depletion

Cited by 4 publications

References 13 publications

Natural killer cell–dependent apoptosis of peripheral murine hematopoietic progenitor cells in response to Fas cross-linking: involvement of tumor necrosis factor-α

Natural killer cell–dependent apoptosis of peripheral murine hematopoietic progenitor cells in response to Fas cross-linking: involvement of tumor necrosis factor-α

IL-12 indirectly enhances proliferation of 5-FU-treated human hematopoietic peripheral blood CD34+ cells

Cell–cell interaction networks regulate blood stem and progenitor cell fate

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