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pubmed-article:7849320pubmed:abstractTextTwo tumor necrosis factor receptors (TNFRs) with molecular weights of 55 kD (TNFR-p55) and 75 kD (TNFR-p75) have recently been identified and cloned. In previous studies, TNFR-p55 has been shown to exclusively mediate bidirectional effects of TNF-alpha on committed bone marrow granulocyte-macrophage progenitor cells, whereas both TNFR-p55 and TNFR-p75 can mediate inhibition of primitive progenitors requiring multiple cytokines to proliferate. We show here that TNF-alpha potently and directly inhibits the in vitro growth of committed erythroid progenitor cells in response to multiple cytokine combinations, and that TNF-alpha-induced inhibition of burst-forming unit-erythroid colony formation is mainly mediated through TNFR-p55, although TNFR-p75-mediated inhibition could be observed on progenitors responsive to erythropoietin alone. Moreover, at low TNF-alpha concentrations (2 ng/mL), TNF-alpha stimulates interleukin-3-dependent in vitro growth of committed granulocyte-macrophage progenitor cells, whereas it potently inhibits erythroid progenitor cell proliferation, showing that one concentration of TNF-alpha can simultaneously and bidirectionally modulate interleukin-3-dependent growth of committed granulocyte-macrophage (stimulation) and erythroid progenitor cells (inhibition).lld:pubmed
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pubmed-article:7849320pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:7849320pubmed:articleTitleTumor necrosis factor (TNF)-alpha directly inhibits human erythropoiesis in vitro: role of p55 and p75 TNF receptors.lld:pubmed
pubmed-article:7849320pubmed:affiliationDepartment of Immunology, Institute for Cancer Research, Norwegian Radium Hospital, Oslo.lld:pubmed
pubmed-article:7849320pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:7849320pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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