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  • Title: Monocytes enhance gamma-interferon-induced inhibition of myeloid progenitor cell growth through secretion of tumor necrosis factor.
    Author: Cannistra SA, Groshek P, Griffin JD.
    Journal: Exp Hematol; 1988 Nov; 16(10):865-70. PubMed ID: 3139436.
    Abstract:
    In this study, we have examined the effects of autologous monocytes and T-lymphocytes on gamma-interferon (gamma-IFN)-induced inhibition of granulocyte-monocyte progenitor cells (CFU-GM) in vitro. Depletion of adherent cells from the mononuclear fraction of normal bone marrow (NBM) resulted in a significant reduction in the inhibitory effects of gamma-IFN on CFU-GM growth, whereas T-lymphocyte depletion had no effect. Adding back autologous monocytes to the underlayer fraction of agar culture resulted in a concentration-dependent enhancement of gamma-IFN-induced CFU-GM inhibition that did not require cell-cell contact. Adding back autologous T-lymphocytes had no effect and did not synergize with monocytes in enhancing gamma-IFN-induced inhibition. Based on the use of indomethacin and the pattern of CFU-GM subset growth, it was determined that prostaglandin E was unlikely to be the humoral inhibitory factor involved in this process. However, the effects of monocytes were completely reversed in the presence of a neutralizing monoclonal antibody to tumor necrosis factor (TNF), suggesting that monocyte-derived TNF was responsible for the enhancement of gamma-IFN-induced CFU-GM inhibition. This observation was further supported by the ability of gamma-IFN to induce an eightfold increase of baseline monocyte TNF secretion in agar culture. These data suggest that gamma-IFN may inhibit progenitor cell growth in vitro through indirect humoral mechanisms involving monocyte-derived TNF, as well as through direct inhibitory effects on CFU-GM proliferation. Because monocytes are a component of the bone marrow microenvironment, the ability of gamma-IFN to induce biologically relevant levels of monocyte-derived TNF may play an important role in the negative regulation of hematopoiesis.
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